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PMC1885946_fig2_11367.jpg | What is the central feature of this picture? | SipA Promotes Salmonella Replication and Is Required for SCV Positioning(A) Upper: Fold increase in intracellular wild-type S. typhimurium (filled circles), the sipA− mutant (sipA−, open squares), and a strain constitutively expressing augmented levels of SipA from a plasmid (sipA++, filled triangles) strain in NIH3T3 cells over time (hr). Equivalent effects were observed in HeLa cells (not shown). Lower: Fold increase (left, RAW264.7 macrophages) or percentage increase compared to wild-type (right, bone marrow-derived macrophages) of wild-type S. typhimurium, the sipA− mutant, and the sipA++ strain over 22 hr. Replication as fold increase in intracellular bacteria was calculated by comparing values at 2 hr and subsequent time points postinfection. NIH3T3 cells were lysed after ∼11 hr due to bacterial replication. Data were derived from three independent experiments and are shown as mean ± SEM.(B) Upper: Typical distribution of wild-type S. typhimurium, the sipA− and ssaV− mutants, and the sipA++ strain (gray) 6 hr after infection of NIH3T3 cells. Lower: The percentage of intracellular bacteria from 50 infected cells proximal (within 3 μm, open bars) and distal (>3 μm, filled bars) to the nearest edge of the nucleus 6 hr postinfection. Positioning and replication of the sipA− strain was rescued by complementation with a low-copy-number plasmid encoding sipA (not shown). Data were derived from three independent experiments and are shown as mean ± SEM.(C) LAMP1 (green) in HeLa cells 6 hr after infection with wild-type S. typhimurium, the sipA− mutant, or the sipA++ or sifA− mutant strains (blue). Scale bar, 5 μm. |
PMC1885946_fig2_11370.jpg | Can you identify the primary element in this image? | SipA Promotes Salmonella Replication and Is Required for SCV Positioning(A) Upper: Fold increase in intracellular wild-type S. typhimurium (filled circles), the sipA− mutant (sipA−, open squares), and a strain constitutively expressing augmented levels of SipA from a plasmid (sipA++, filled triangles) strain in NIH3T3 cells over time (hr). Equivalent effects were observed in HeLa cells (not shown). Lower: Fold increase (left, RAW264.7 macrophages) or percentage increase compared to wild-type (right, bone marrow-derived macrophages) of wild-type S. typhimurium, the sipA− mutant, and the sipA++ strain over 22 hr. Replication as fold increase in intracellular bacteria was calculated by comparing values at 2 hr and subsequent time points postinfection. NIH3T3 cells were lysed after ∼11 hr due to bacterial replication. Data were derived from three independent experiments and are shown as mean ± SEM.(B) Upper: Typical distribution of wild-type S. typhimurium, the sipA− and ssaV− mutants, and the sipA++ strain (gray) 6 hr after infection of NIH3T3 cells. Lower: The percentage of intracellular bacteria from 50 infected cells proximal (within 3 μm, open bars) and distal (>3 μm, filled bars) to the nearest edge of the nucleus 6 hr postinfection. Positioning and replication of the sipA− strain was rescued by complementation with a low-copy-number plasmid encoding sipA (not shown). Data were derived from three independent experiments and are shown as mean ± SEM.(C) LAMP1 (green) in HeLa cells 6 hr after infection with wild-type S. typhimurium, the sipA− mutant, or the sipA++ or sifA− mutant strains (blue). Scale bar, 5 μm. |
PMC1885946_fig2_11364.jpg | What is the central feature of this picture? | SipA Promotes Salmonella Replication and Is Required for SCV Positioning(A) Upper: Fold increase in intracellular wild-type S. typhimurium (filled circles), the sipA− mutant (sipA−, open squares), and a strain constitutively expressing augmented levels of SipA from a plasmid (sipA++, filled triangles) strain in NIH3T3 cells over time (hr). Equivalent effects were observed in HeLa cells (not shown). Lower: Fold increase (left, RAW264.7 macrophages) or percentage increase compared to wild-type (right, bone marrow-derived macrophages) of wild-type S. typhimurium, the sipA− mutant, and the sipA++ strain over 22 hr. Replication as fold increase in intracellular bacteria was calculated by comparing values at 2 hr and subsequent time points postinfection. NIH3T3 cells were lysed after ∼11 hr due to bacterial replication. Data were derived from three independent experiments and are shown as mean ± SEM.(B) Upper: Typical distribution of wild-type S. typhimurium, the sipA− and ssaV− mutants, and the sipA++ strain (gray) 6 hr after infection of NIH3T3 cells. Lower: The percentage of intracellular bacteria from 50 infected cells proximal (within 3 μm, open bars) and distal (>3 μm, filled bars) to the nearest edge of the nucleus 6 hr postinfection. Positioning and replication of the sipA− strain was rescued by complementation with a low-copy-number plasmid encoding sipA (not shown). Data were derived from three independent experiments and are shown as mean ± SEM.(C) LAMP1 (green) in HeLa cells 6 hr after infection with wild-type S. typhimurium, the sipA− mutant, or the sipA++ or sifA− mutant strains (blue). Scale bar, 5 μm. |
PMC1885946_fig2_11372.jpg | What object or scene is depicted here? | SipA Promotes Salmonella Replication and Is Required for SCV Positioning(A) Upper: Fold increase in intracellular wild-type S. typhimurium (filled circles), the sipA− mutant (sipA−, open squares), and a strain constitutively expressing augmented levels of SipA from a plasmid (sipA++, filled triangles) strain in NIH3T3 cells over time (hr). Equivalent effects were observed in HeLa cells (not shown). Lower: Fold increase (left, RAW264.7 macrophages) or percentage increase compared to wild-type (right, bone marrow-derived macrophages) of wild-type S. typhimurium, the sipA− mutant, and the sipA++ strain over 22 hr. Replication as fold increase in intracellular bacteria was calculated by comparing values at 2 hr and subsequent time points postinfection. NIH3T3 cells were lysed after ∼11 hr due to bacterial replication. Data were derived from three independent experiments and are shown as mean ± SEM.(B) Upper: Typical distribution of wild-type S. typhimurium, the sipA− and ssaV− mutants, and the sipA++ strain (gray) 6 hr after infection of NIH3T3 cells. Lower: The percentage of intracellular bacteria from 50 infected cells proximal (within 3 μm, open bars) and distal (>3 μm, filled bars) to the nearest edge of the nucleus 6 hr postinfection. Positioning and replication of the sipA− strain was rescued by complementation with a low-copy-number plasmid encoding sipA (not shown). Data were derived from three independent experiments and are shown as mean ± SEM.(C) LAMP1 (green) in HeLa cells 6 hr after infection with wild-type S. typhimurium, the sipA− mutant, or the sipA++ or sifA− mutant strains (blue). Scale bar, 5 μm. |
PMC1885946_fig2_11363.jpg | What is the principal component of this image? | SipA Promotes Salmonella Replication and Is Required for SCV Positioning(A) Upper: Fold increase in intracellular wild-type S. typhimurium (filled circles), the sipA− mutant (sipA−, open squares), and a strain constitutively expressing augmented levels of SipA from a plasmid (sipA++, filled triangles) strain in NIH3T3 cells over time (hr). Equivalent effects were observed in HeLa cells (not shown). Lower: Fold increase (left, RAW264.7 macrophages) or percentage increase compared to wild-type (right, bone marrow-derived macrophages) of wild-type S. typhimurium, the sipA− mutant, and the sipA++ strain over 22 hr. Replication as fold increase in intracellular bacteria was calculated by comparing values at 2 hr and subsequent time points postinfection. NIH3T3 cells were lysed after ∼11 hr due to bacterial replication. Data were derived from three independent experiments and are shown as mean ± SEM.(B) Upper: Typical distribution of wild-type S. typhimurium, the sipA− and ssaV− mutants, and the sipA++ strain (gray) 6 hr after infection of NIH3T3 cells. Lower: The percentage of intracellular bacteria from 50 infected cells proximal (within 3 μm, open bars) and distal (>3 μm, filled bars) to the nearest edge of the nucleus 6 hr postinfection. Positioning and replication of the sipA− strain was rescued by complementation with a low-copy-number plasmid encoding sipA (not shown). Data were derived from three independent experiments and are shown as mean ± SEM.(C) LAMP1 (green) in HeLa cells 6 hr after infection with wild-type S. typhimurium, the sipA− mutant, or the sipA++ or sifA− mutant strains (blue). Scale bar, 5 μm. |
PMC1885946_fig3_11399.jpg | What is being portrayed in this visual content? | SipA Simultaneously Promotes Perinuclear SCV Migration and Prevents Kinesin Association(A) Dynein and conventional kinesin (red) in NIH3T3 cells 6 hr after infection with wild-type S. typhimurium or the sipA− mutant (blue). Scale bars, 3 μm (kinesin) and 5 μm (dynein).(B) Deconvolved immunofluorescence micrographs of a single z section from a rendered image showing NIH3T3 cells 6 hr postinfection with wild-type S. typhimurium or the sipA− mutant (blue). Scale bars, 5 μm. Colocalization between kinesin (red), tubulin (green), and the sipA− mutant is marked with arrows. Indicated regions are rotated 180° about the x (x180) and y (y180) axes.(C) Upper: Typical distribution of wild-type S. typhimurium and the sipA− mutant (red [left] or blue [right]) 6 hr after infection of pGFP-p50/dynamitin-transfected (left) or ATA-treated (right) NIH3T3 cells. Scale bar, 5 μm. Lower: The percentage of bacteria proximal (<3 μm, open bars) and distal (>3 μm, filled bars) to the nearest edge of the nucleus in pGFP-p50/dynamitin-transfected (left) and ATA-treated (right) NIH3T3 cells. Data were derived from three independent experiments and are shown as mean ± SEM. |
PMC1885946_fig3_11395.jpg | What is the central feature of this picture? | SipA Simultaneously Promotes Perinuclear SCV Migration and Prevents Kinesin Association(A) Dynein and conventional kinesin (red) in NIH3T3 cells 6 hr after infection with wild-type S. typhimurium or the sipA− mutant (blue). Scale bars, 3 μm (kinesin) and 5 μm (dynein).(B) Deconvolved immunofluorescence micrographs of a single z section from a rendered image showing NIH3T3 cells 6 hr postinfection with wild-type S. typhimurium or the sipA− mutant (blue). Scale bars, 5 μm. Colocalization between kinesin (red), tubulin (green), and the sipA− mutant is marked with arrows. Indicated regions are rotated 180° about the x (x180) and y (y180) axes.(C) Upper: Typical distribution of wild-type S. typhimurium and the sipA− mutant (red [left] or blue [right]) 6 hr after infection of pGFP-p50/dynamitin-transfected (left) or ATA-treated (right) NIH3T3 cells. Scale bar, 5 μm. Lower: The percentage of bacteria proximal (<3 μm, open bars) and distal (>3 μm, filled bars) to the nearest edge of the nucleus in pGFP-p50/dynamitin-transfected (left) and ATA-treated (right) NIH3T3 cells. Data were derived from three independent experiments and are shown as mean ± SEM. |
PMC1885946_fig3_11397.jpg | Describe the main subject of this image. | SipA Simultaneously Promotes Perinuclear SCV Migration and Prevents Kinesin Association(A) Dynein and conventional kinesin (red) in NIH3T3 cells 6 hr after infection with wild-type S. typhimurium or the sipA− mutant (blue). Scale bars, 3 μm (kinesin) and 5 μm (dynein).(B) Deconvolved immunofluorescence micrographs of a single z section from a rendered image showing NIH3T3 cells 6 hr postinfection with wild-type S. typhimurium or the sipA− mutant (blue). Scale bars, 5 μm. Colocalization between kinesin (red), tubulin (green), and the sipA− mutant is marked with arrows. Indicated regions are rotated 180° about the x (x180) and y (y180) axes.(C) Upper: Typical distribution of wild-type S. typhimurium and the sipA− mutant (red [left] or blue [right]) 6 hr after infection of pGFP-p50/dynamitin-transfected (left) or ATA-treated (right) NIH3T3 cells. Scale bar, 5 μm. Lower: The percentage of bacteria proximal (<3 μm, open bars) and distal (>3 μm, filled bars) to the nearest edge of the nucleus in pGFP-p50/dynamitin-transfected (left) and ATA-treated (right) NIH3T3 cells. Data were derived from three independent experiments and are shown as mean ± SEM. |
PMC1885946_fig3_11396.jpg | What is the focal point of this photograph? | SipA Simultaneously Promotes Perinuclear SCV Migration and Prevents Kinesin Association(A) Dynein and conventional kinesin (red) in NIH3T3 cells 6 hr after infection with wild-type S. typhimurium or the sipA− mutant (blue). Scale bars, 3 μm (kinesin) and 5 μm (dynein).(B) Deconvolved immunofluorescence micrographs of a single z section from a rendered image showing NIH3T3 cells 6 hr postinfection with wild-type S. typhimurium or the sipA− mutant (blue). Scale bars, 5 μm. Colocalization between kinesin (red), tubulin (green), and the sipA− mutant is marked with arrows. Indicated regions are rotated 180° about the x (x180) and y (y180) axes.(C) Upper: Typical distribution of wild-type S. typhimurium and the sipA− mutant (red [left] or blue [right]) 6 hr after infection of pGFP-p50/dynamitin-transfected (left) or ATA-treated (right) NIH3T3 cells. Scale bar, 5 μm. Lower: The percentage of bacteria proximal (<3 μm, open bars) and distal (>3 μm, filled bars) to the nearest edge of the nucleus in pGFP-p50/dynamitin-transfected (left) and ATA-treated (right) NIH3T3 cells. Data were derived from three independent experiments and are shown as mean ± SEM. |
PMC1885946_fig3_11401.jpg | What is the core subject represented in this visual? | SipA Simultaneously Promotes Perinuclear SCV Migration and Prevents Kinesin Association(A) Dynein and conventional kinesin (red) in NIH3T3 cells 6 hr after infection with wild-type S. typhimurium or the sipA− mutant (blue). Scale bars, 3 μm (kinesin) and 5 μm (dynein).(B) Deconvolved immunofluorescence micrographs of a single z section from a rendered image showing NIH3T3 cells 6 hr postinfection with wild-type S. typhimurium or the sipA− mutant (blue). Scale bars, 5 μm. Colocalization between kinesin (red), tubulin (green), and the sipA− mutant is marked with arrows. Indicated regions are rotated 180° about the x (x180) and y (y180) axes.(C) Upper: Typical distribution of wild-type S. typhimurium and the sipA− mutant (red [left] or blue [right]) 6 hr after infection of pGFP-p50/dynamitin-transfected (left) or ATA-treated (right) NIH3T3 cells. Scale bar, 5 μm. Lower: The percentage of bacteria proximal (<3 μm, open bars) and distal (>3 μm, filled bars) to the nearest edge of the nucleus in pGFP-p50/dynamitin-transfected (left) and ATA-treated (right) NIH3T3 cells. Data were derived from three independent experiments and are shown as mean ± SEM. |
PMC1885946_fig3_11400.jpg | What object or scene is depicted here? | SipA Simultaneously Promotes Perinuclear SCV Migration and Prevents Kinesin Association(A) Dynein and conventional kinesin (red) in NIH3T3 cells 6 hr after infection with wild-type S. typhimurium or the sipA− mutant (blue). Scale bars, 3 μm (kinesin) and 5 μm (dynein).(B) Deconvolved immunofluorescence micrographs of a single z section from a rendered image showing NIH3T3 cells 6 hr postinfection with wild-type S. typhimurium or the sipA− mutant (blue). Scale bars, 5 μm. Colocalization between kinesin (red), tubulin (green), and the sipA− mutant is marked with arrows. Indicated regions are rotated 180° about the x (x180) and y (y180) axes.(C) Upper: Typical distribution of wild-type S. typhimurium and the sipA− mutant (red [left] or blue [right]) 6 hr after infection of pGFP-p50/dynamitin-transfected (left) or ATA-treated (right) NIH3T3 cells. Scale bar, 5 μm. Lower: The percentage of bacteria proximal (<3 μm, open bars) and distal (>3 μm, filled bars) to the nearest edge of the nucleus in pGFP-p50/dynamitin-transfected (left) and ATA-treated (right) NIH3T3 cells. Data were derived from three independent experiments and are shown as mean ± SEM. |
PMC1885946_fig3_11391.jpg | What is the main focus of this visual representation? | SipA Simultaneously Promotes Perinuclear SCV Migration and Prevents Kinesin Association(A) Dynein and conventional kinesin (red) in NIH3T3 cells 6 hr after infection with wild-type S. typhimurium or the sipA− mutant (blue). Scale bars, 3 μm (kinesin) and 5 μm (dynein).(B) Deconvolved immunofluorescence micrographs of a single z section from a rendered image showing NIH3T3 cells 6 hr postinfection with wild-type S. typhimurium or the sipA− mutant (blue). Scale bars, 5 μm. Colocalization between kinesin (red), tubulin (green), and the sipA− mutant is marked with arrows. Indicated regions are rotated 180° about the x (x180) and y (y180) axes.(C) Upper: Typical distribution of wild-type S. typhimurium and the sipA− mutant (red [left] or blue [right]) 6 hr after infection of pGFP-p50/dynamitin-transfected (left) or ATA-treated (right) NIH3T3 cells. Scale bar, 5 μm. Lower: The percentage of bacteria proximal (<3 μm, open bars) and distal (>3 μm, filled bars) to the nearest edge of the nucleus in pGFP-p50/dynamitin-transfected (left) and ATA-treated (right) NIH3T3 cells. Data were derived from three independent experiments and are shown as mean ± SEM. |
PMC1885946_fig3_11398.jpg | What key item or scene is captured in this photo? | SipA Simultaneously Promotes Perinuclear SCV Migration and Prevents Kinesin Association(A) Dynein and conventional kinesin (red) in NIH3T3 cells 6 hr after infection with wild-type S. typhimurium or the sipA− mutant (blue). Scale bars, 3 μm (kinesin) and 5 μm (dynein).(B) Deconvolved immunofluorescence micrographs of a single z section from a rendered image showing NIH3T3 cells 6 hr postinfection with wild-type S. typhimurium or the sipA− mutant (blue). Scale bars, 5 μm. Colocalization between kinesin (red), tubulin (green), and the sipA− mutant is marked with arrows. Indicated regions are rotated 180° about the x (x180) and y (y180) axes.(C) Upper: Typical distribution of wild-type S. typhimurium and the sipA− mutant (red [left] or blue [right]) 6 hr after infection of pGFP-p50/dynamitin-transfected (left) or ATA-treated (right) NIH3T3 cells. Scale bar, 5 μm. Lower: The percentage of bacteria proximal (<3 μm, open bars) and distal (>3 μm, filled bars) to the nearest edge of the nucleus in pGFP-p50/dynamitin-transfected (left) and ATA-treated (right) NIH3T3 cells. Data were derived from three independent experiments and are shown as mean ± SEM. |
PMC1885946_fig3_11392.jpg | What's the most prominent thing you notice in this picture? | SipA Simultaneously Promotes Perinuclear SCV Migration and Prevents Kinesin Association(A) Dynein and conventional kinesin (red) in NIH3T3 cells 6 hr after infection with wild-type S. typhimurium or the sipA− mutant (blue). Scale bars, 3 μm (kinesin) and 5 μm (dynein).(B) Deconvolved immunofluorescence micrographs of a single z section from a rendered image showing NIH3T3 cells 6 hr postinfection with wild-type S. typhimurium or the sipA− mutant (blue). Scale bars, 5 μm. Colocalization between kinesin (red), tubulin (green), and the sipA− mutant is marked with arrows. Indicated regions are rotated 180° about the x (x180) and y (y180) axes.(C) Upper: Typical distribution of wild-type S. typhimurium and the sipA− mutant (red [left] or blue [right]) 6 hr after infection of pGFP-p50/dynamitin-transfected (left) or ATA-treated (right) NIH3T3 cells. Scale bar, 5 μm. Lower: The percentage of bacteria proximal (<3 μm, open bars) and distal (>3 μm, filled bars) to the nearest edge of the nucleus in pGFP-p50/dynamitin-transfected (left) and ATA-treated (right) NIH3T3 cells. Data were derived from three independent experiments and are shown as mean ± SEM. |
PMC1885946_fig5_11387.jpg | What is the dominant medical problem in this image? | The N-Terminal Region of SipA Induces Centripetal Redistribution of Late Endosomes toward the Microtubule-Organizing Center(A) Upper: CFP-SipA, CFP-SipA-N, and CFP-SipA-C (green) NIH3T3 transfectants costained for F-actin (red). Equivalent localization was observed for comparable YFP fusions and SipA, SipA-N, and SipA-C. Scale bar, 5 μm. Lower: NIH3T3 transfectants were mechanically fractionated. Nuclear (N), internal membrane/cytoskeleton (IM/CS), cytosol (C), and plasma membrane (PM) fractions were analyzed by anti-SipA immunoblotting.(B) LAMP1 (red) and tubulin (green) localization in NIH3T3 transfectants expressing SipA, SipA-N, or SipA-C. “M” indicates microtubule-organizing center. Scale bar, 5 μm. Lower panels show perinuclear colocalization of CFP-SipA-N and LAMP1. Scale bars, 5 μm. |
PMC1885946_fig5_11381.jpg | Can you identify the primary element in this image? | The N-Terminal Region of SipA Induces Centripetal Redistribution of Late Endosomes toward the Microtubule-Organizing Center(A) Upper: CFP-SipA, CFP-SipA-N, and CFP-SipA-C (green) NIH3T3 transfectants costained for F-actin (red). Equivalent localization was observed for comparable YFP fusions and SipA, SipA-N, and SipA-C. Scale bar, 5 μm. Lower: NIH3T3 transfectants were mechanically fractionated. Nuclear (N), internal membrane/cytoskeleton (IM/CS), cytosol (C), and plasma membrane (PM) fractions were analyzed by anti-SipA immunoblotting.(B) LAMP1 (red) and tubulin (green) localization in NIH3T3 transfectants expressing SipA, SipA-N, or SipA-C. “M” indicates microtubule-organizing center. Scale bar, 5 μm. Lower panels show perinuclear colocalization of CFP-SipA-N and LAMP1. Scale bars, 5 μm. |
PMC1885946_fig5_11386.jpg | What is shown in this image? | The N-Terminal Region of SipA Induces Centripetal Redistribution of Late Endosomes toward the Microtubule-Organizing Center(A) Upper: CFP-SipA, CFP-SipA-N, and CFP-SipA-C (green) NIH3T3 transfectants costained for F-actin (red). Equivalent localization was observed for comparable YFP fusions and SipA, SipA-N, and SipA-C. Scale bar, 5 μm. Lower: NIH3T3 transfectants were mechanically fractionated. Nuclear (N), internal membrane/cytoskeleton (IM/CS), cytosol (C), and plasma membrane (PM) fractions were analyzed by anti-SipA immunoblotting.(B) LAMP1 (red) and tubulin (green) localization in NIH3T3 transfectants expressing SipA, SipA-N, or SipA-C. “M” indicates microtubule-organizing center. Scale bar, 5 μm. Lower panels show perinuclear colocalization of CFP-SipA-N and LAMP1. Scale bars, 5 μm. |
PMC1885946_fig5_11380.jpg | What key item or scene is captured in this photo? | The N-Terminal Region of SipA Induces Centripetal Redistribution of Late Endosomes toward the Microtubule-Organizing Center(A) Upper: CFP-SipA, CFP-SipA-N, and CFP-SipA-C (green) NIH3T3 transfectants costained for F-actin (red). Equivalent localization was observed for comparable YFP fusions and SipA, SipA-N, and SipA-C. Scale bar, 5 μm. Lower: NIH3T3 transfectants were mechanically fractionated. Nuclear (N), internal membrane/cytoskeleton (IM/CS), cytosol (C), and plasma membrane (PM) fractions were analyzed by anti-SipA immunoblotting.(B) LAMP1 (red) and tubulin (green) localization in NIH3T3 transfectants expressing SipA, SipA-N, or SipA-C. “M” indicates microtubule-organizing center. Scale bar, 5 μm. Lower panels show perinuclear colocalization of CFP-SipA-N and LAMP1. Scale bars, 5 μm. |
PMC1885946_fig5_11384.jpg | Can you identify the primary element in this image? | The N-Terminal Region of SipA Induces Centripetal Redistribution of Late Endosomes toward the Microtubule-Organizing Center(A) Upper: CFP-SipA, CFP-SipA-N, and CFP-SipA-C (green) NIH3T3 transfectants costained for F-actin (red). Equivalent localization was observed for comparable YFP fusions and SipA, SipA-N, and SipA-C. Scale bar, 5 μm. Lower: NIH3T3 transfectants were mechanically fractionated. Nuclear (N), internal membrane/cytoskeleton (IM/CS), cytosol (C), and plasma membrane (PM) fractions were analyzed by anti-SipA immunoblotting.(B) LAMP1 (red) and tubulin (green) localization in NIH3T3 transfectants expressing SipA, SipA-N, or SipA-C. “M” indicates microtubule-organizing center. Scale bar, 5 μm. Lower panels show perinuclear colocalization of CFP-SipA-N and LAMP1. Scale bars, 5 μm. |
PMC1885946_fig5_11385.jpg | What stands out most in this visual? | The N-Terminal Region of SipA Induces Centripetal Redistribution of Late Endosomes toward the Microtubule-Organizing Center(A) Upper: CFP-SipA, CFP-SipA-N, and CFP-SipA-C (green) NIH3T3 transfectants costained for F-actin (red). Equivalent localization was observed for comparable YFP fusions and SipA, SipA-N, and SipA-C. Scale bar, 5 μm. Lower: NIH3T3 transfectants were mechanically fractionated. Nuclear (N), internal membrane/cytoskeleton (IM/CS), cytosol (C), and plasma membrane (PM) fractions were analyzed by anti-SipA immunoblotting.(B) LAMP1 (red) and tubulin (green) localization in NIH3T3 transfectants expressing SipA, SipA-N, or SipA-C. “M” indicates microtubule-organizing center. Scale bar, 5 μm. Lower panels show perinuclear colocalization of CFP-SipA-N and LAMP1. Scale bars, 5 μm. |
PMC1885946_fig5_11389.jpg | What is the dominant medical problem in this image? | The N-Terminal Region of SipA Induces Centripetal Redistribution of Late Endosomes toward the Microtubule-Organizing Center(A) Upper: CFP-SipA, CFP-SipA-N, and CFP-SipA-C (green) NIH3T3 transfectants costained for F-actin (red). Equivalent localization was observed for comparable YFP fusions and SipA, SipA-N, and SipA-C. Scale bar, 5 μm. Lower: NIH3T3 transfectants were mechanically fractionated. Nuclear (N), internal membrane/cytoskeleton (IM/CS), cytosol (C), and plasma membrane (PM) fractions were analyzed by anti-SipA immunoblotting.(B) LAMP1 (red) and tubulin (green) localization in NIH3T3 transfectants expressing SipA, SipA-N, or SipA-C. “M” indicates microtubule-organizing center. Scale bar, 5 μm. Lower panels show perinuclear colocalization of CFP-SipA-N and LAMP1. Scale bars, 5 μm. |
PMC1885946_fig5_11383.jpg | What is the principal component of this image? | The N-Terminal Region of SipA Induces Centripetal Redistribution of Late Endosomes toward the Microtubule-Organizing Center(A) Upper: CFP-SipA, CFP-SipA-N, and CFP-SipA-C (green) NIH3T3 transfectants costained for F-actin (red). Equivalent localization was observed for comparable YFP fusions and SipA, SipA-N, and SipA-C. Scale bar, 5 μm. Lower: NIH3T3 transfectants were mechanically fractionated. Nuclear (N), internal membrane/cytoskeleton (IM/CS), cytosol (C), and plasma membrane (PM) fractions were analyzed by anti-SipA immunoblotting.(B) LAMP1 (red) and tubulin (green) localization in NIH3T3 transfectants expressing SipA, SipA-N, or SipA-C. “M” indicates microtubule-organizing center. Scale bar, 5 μm. Lower panels show perinuclear colocalization of CFP-SipA-N and LAMP1. Scale bars, 5 μm. |
PMC1885946_fig5_11388.jpg | What is the dominant medical problem in this image? | The N-Terminal Region of SipA Induces Centripetal Redistribution of Late Endosomes toward the Microtubule-Organizing Center(A) Upper: CFP-SipA, CFP-SipA-N, and CFP-SipA-C (green) NIH3T3 transfectants costained for F-actin (red). Equivalent localization was observed for comparable YFP fusions and SipA, SipA-N, and SipA-C. Scale bar, 5 μm. Lower: NIH3T3 transfectants were mechanically fractionated. Nuclear (N), internal membrane/cytoskeleton (IM/CS), cytosol (C), and plasma membrane (PM) fractions were analyzed by anti-SipA immunoblotting.(B) LAMP1 (red) and tubulin (green) localization in NIH3T3 transfectants expressing SipA, SipA-N, or SipA-C. “M” indicates microtubule-organizing center. Scale bar, 5 μm. Lower panels show perinuclear colocalization of CFP-SipA-N and LAMP1. Scale bars, 5 μm. |
PMC1885946_fig5_11382.jpg | What is the core subject represented in this visual? | The N-Terminal Region of SipA Induces Centripetal Redistribution of Late Endosomes toward the Microtubule-Organizing Center(A) Upper: CFP-SipA, CFP-SipA-N, and CFP-SipA-C (green) NIH3T3 transfectants costained for F-actin (red). Equivalent localization was observed for comparable YFP fusions and SipA, SipA-N, and SipA-C. Scale bar, 5 μm. Lower: NIH3T3 transfectants were mechanically fractionated. Nuclear (N), internal membrane/cytoskeleton (IM/CS), cytosol (C), and plasma membrane (PM) fractions were analyzed by anti-SipA immunoblotting.(B) LAMP1 (red) and tubulin (green) localization in NIH3T3 transfectants expressing SipA, SipA-N, or SipA-C. “M” indicates microtubule-organizing center. Scale bar, 5 μm. Lower panels show perinuclear colocalization of CFP-SipA-N and LAMP1. Scale bars, 5 μm. |
PMC1885946_fig5_11378.jpg | What key item or scene is captured in this photo? | The N-Terminal Region of SipA Induces Centripetal Redistribution of Late Endosomes toward the Microtubule-Organizing Center(A) Upper: CFP-SipA, CFP-SipA-N, and CFP-SipA-C (green) NIH3T3 transfectants costained for F-actin (red). Equivalent localization was observed for comparable YFP fusions and SipA, SipA-N, and SipA-C. Scale bar, 5 μm. Lower: NIH3T3 transfectants were mechanically fractionated. Nuclear (N), internal membrane/cytoskeleton (IM/CS), cytosol (C), and plasma membrane (PM) fractions were analyzed by anti-SipA immunoblotting.(B) LAMP1 (red) and tubulin (green) localization in NIH3T3 transfectants expressing SipA, SipA-N, or SipA-C. “M” indicates microtubule-organizing center. Scale bar, 5 μm. Lower panels show perinuclear colocalization of CFP-SipA-N and LAMP1. Scale bars, 5 μm. |
PMC1885946_fig5_11377.jpg | What can you see in this picture? | The N-Terminal Region of SipA Induces Centripetal Redistribution of Late Endosomes toward the Microtubule-Organizing Center(A) Upper: CFP-SipA, CFP-SipA-N, and CFP-SipA-C (green) NIH3T3 transfectants costained for F-actin (red). Equivalent localization was observed for comparable YFP fusions and SipA, SipA-N, and SipA-C. Scale bar, 5 μm. Lower: NIH3T3 transfectants were mechanically fractionated. Nuclear (N), internal membrane/cytoskeleton (IM/CS), cytosol (C), and plasma membrane (PM) fractions were analyzed by anti-SipA immunoblotting.(B) LAMP1 (red) and tubulin (green) localization in NIH3T3 transfectants expressing SipA, SipA-N, or SipA-C. “M” indicates microtubule-organizing center. Scale bar, 5 μm. Lower panels show perinuclear colocalization of CFP-SipA-N and LAMP1. Scale bars, 5 μm. |
PMC1885946_fig5_11376.jpg | What's the most prominent thing you notice in this picture? | The N-Terminal Region of SipA Induces Centripetal Redistribution of Late Endosomes toward the Microtubule-Organizing Center(A) Upper: CFP-SipA, CFP-SipA-N, and CFP-SipA-C (green) NIH3T3 transfectants costained for F-actin (red). Equivalent localization was observed for comparable YFP fusions and SipA, SipA-N, and SipA-C. Scale bar, 5 μm. Lower: NIH3T3 transfectants were mechanically fractionated. Nuclear (N), internal membrane/cytoskeleton (IM/CS), cytosol (C), and plasma membrane (PM) fractions were analyzed by anti-SipA immunoblotting.(B) LAMP1 (red) and tubulin (green) localization in NIH3T3 transfectants expressing SipA, SipA-N, or SipA-C. “M” indicates microtubule-organizing center. Scale bar, 5 μm. Lower panels show perinuclear colocalization of CFP-SipA-N and LAMP1. Scale bars, 5 μm. |
PMC1885946_fig5_11390.jpg | What is the main focus of this visual representation? | The N-Terminal Region of SipA Induces Centripetal Redistribution of Late Endosomes toward the Microtubule-Organizing Center(A) Upper: CFP-SipA, CFP-SipA-N, and CFP-SipA-C (green) NIH3T3 transfectants costained for F-actin (red). Equivalent localization was observed for comparable YFP fusions and SipA, SipA-N, and SipA-C. Scale bar, 5 μm. Lower: NIH3T3 transfectants were mechanically fractionated. Nuclear (N), internal membrane/cytoskeleton (IM/CS), cytosol (C), and plasma membrane (PM) fractions were analyzed by anti-SipA immunoblotting.(B) LAMP1 (red) and tubulin (green) localization in NIH3T3 transfectants expressing SipA, SipA-N, or SipA-C. “M” indicates microtubule-organizing center. Scale bar, 5 μm. Lower panels show perinuclear colocalization of CFP-SipA-N and LAMP1. Scale bars, 5 μm. |
PMC1885946_fig5_11379.jpg | What is being portrayed in this visual content? | The N-Terminal Region of SipA Induces Centripetal Redistribution of Late Endosomes toward the Microtubule-Organizing Center(A) Upper: CFP-SipA, CFP-SipA-N, and CFP-SipA-C (green) NIH3T3 transfectants costained for F-actin (red). Equivalent localization was observed for comparable YFP fusions and SipA, SipA-N, and SipA-C. Scale bar, 5 μm. Lower: NIH3T3 transfectants were mechanically fractionated. Nuclear (N), internal membrane/cytoskeleton (IM/CS), cytosol (C), and plasma membrane (PM) fractions were analyzed by anti-SipA immunoblotting.(B) LAMP1 (red) and tubulin (green) localization in NIH3T3 transfectants expressing SipA, SipA-N, or SipA-C. “M” indicates microtubule-organizing center. Scale bar, 5 μm. Lower panels show perinuclear colocalization of CFP-SipA-N and LAMP1. Scale bars, 5 μm. |
PMC1885946_fig5_11375.jpg | What is the core subject represented in this visual? | The N-Terminal Region of SipA Induces Centripetal Redistribution of Late Endosomes toward the Microtubule-Organizing Center(A) Upper: CFP-SipA, CFP-SipA-N, and CFP-SipA-C (green) NIH3T3 transfectants costained for F-actin (red). Equivalent localization was observed for comparable YFP fusions and SipA, SipA-N, and SipA-C. Scale bar, 5 μm. Lower: NIH3T3 transfectants were mechanically fractionated. Nuclear (N), internal membrane/cytoskeleton (IM/CS), cytosol (C), and plasma membrane (PM) fractions were analyzed by anti-SipA immunoblotting.(B) LAMP1 (red) and tubulin (green) localization in NIH3T3 transfectants expressing SipA, SipA-N, or SipA-C. “M” indicates microtubule-organizing center. Scale bar, 5 μm. Lower panels show perinuclear colocalization of CFP-SipA-N and LAMP1. Scale bars, 5 μm. |
PMC1885951_fig2_11407.jpg | What is the core subject represented in this visual? | Markers for the Plus Ends of Microtubules Colocalize with Ectopic oskar mRNA(A–C) A wild-type egg chamber; Kin:β-GAL (A) localizes to the posterior pole of the oocyte at stage 9 and colocalizes with Staufen (B).(D–F) A UAS-osk egg chamber; Kin:β-GAL (D) and Staufen (E) are mislocalized to a dot in the center of the oocytes with overexpressed oskar mRNA, as well as to the posterior pole.(G–L) Dynamitin:GFP (G) fusion protein localizes to the posterior pole in wild-type egg chambers and colocalize with pole-plasm markers, such as Stau (H). In UAS-osk flies, Dynamitin:GFP (J) and Stau (K) are mislocalized to the ectopic site in the middle of the oocyte. |
PMC1885951_fig2_11403.jpg | Describe the main subject of this image. | Markers for the Plus Ends of Microtubules Colocalize with Ectopic oskar mRNA(A–C) A wild-type egg chamber; Kin:β-GAL (A) localizes to the posterior pole of the oocyte at stage 9 and colocalizes with Staufen (B).(D–F) A UAS-osk egg chamber; Kin:β-GAL (D) and Staufen (E) are mislocalized to a dot in the center of the oocytes with overexpressed oskar mRNA, as well as to the posterior pole.(G–L) Dynamitin:GFP (G) fusion protein localizes to the posterior pole in wild-type egg chambers and colocalize with pole-plasm markers, such as Stau (H). In UAS-osk flies, Dynamitin:GFP (J) and Stau (K) are mislocalized to the ectopic site in the middle of the oocyte. |
PMC1885951_fig2_11410.jpg | What does this image primarily show? | Markers for the Plus Ends of Microtubules Colocalize with Ectopic oskar mRNA(A–C) A wild-type egg chamber; Kin:β-GAL (A) localizes to the posterior pole of the oocyte at stage 9 and colocalizes with Staufen (B).(D–F) A UAS-osk egg chamber; Kin:β-GAL (D) and Staufen (E) are mislocalized to a dot in the center of the oocytes with overexpressed oskar mRNA, as well as to the posterior pole.(G–L) Dynamitin:GFP (G) fusion protein localizes to the posterior pole in wild-type egg chambers and colocalize with pole-plasm markers, such as Stau (H). In UAS-osk flies, Dynamitin:GFP (J) and Stau (K) are mislocalized to the ectopic site in the middle of the oocyte. |
PMC1885951_fig2_11408.jpg | What can you see in this picture? | Markers for the Plus Ends of Microtubules Colocalize with Ectopic oskar mRNA(A–C) A wild-type egg chamber; Kin:β-GAL (A) localizes to the posterior pole of the oocyte at stage 9 and colocalizes with Staufen (B).(D–F) A UAS-osk egg chamber; Kin:β-GAL (D) and Staufen (E) are mislocalized to a dot in the center of the oocytes with overexpressed oskar mRNA, as well as to the posterior pole.(G–L) Dynamitin:GFP (G) fusion protein localizes to the posterior pole in wild-type egg chambers and colocalize with pole-plasm markers, such as Stau (H). In UAS-osk flies, Dynamitin:GFP (J) and Stau (K) are mislocalized to the ectopic site in the middle of the oocyte. |
PMC1885951_fig2_11406.jpg | What is the core subject represented in this visual? | Markers for the Plus Ends of Microtubules Colocalize with Ectopic oskar mRNA(A–C) A wild-type egg chamber; Kin:β-GAL (A) localizes to the posterior pole of the oocyte at stage 9 and colocalizes with Staufen (B).(D–F) A UAS-osk egg chamber; Kin:β-GAL (D) and Staufen (E) are mislocalized to a dot in the center of the oocytes with overexpressed oskar mRNA, as well as to the posterior pole.(G–L) Dynamitin:GFP (G) fusion protein localizes to the posterior pole in wild-type egg chambers and colocalize with pole-plasm markers, such as Stau (H). In UAS-osk flies, Dynamitin:GFP (J) and Stau (K) are mislocalized to the ectopic site in the middle of the oocyte. |
PMC1885951_fig2_11412.jpg | What can you see in this picture? | Markers for the Plus Ends of Microtubules Colocalize with Ectopic oskar mRNA(A–C) A wild-type egg chamber; Kin:β-GAL (A) localizes to the posterior pole of the oocyte at stage 9 and colocalizes with Staufen (B).(D–F) A UAS-osk egg chamber; Kin:β-GAL (D) and Staufen (E) are mislocalized to a dot in the center of the oocytes with overexpressed oskar mRNA, as well as to the posterior pole.(G–L) Dynamitin:GFP (G) fusion protein localizes to the posterior pole in wild-type egg chambers and colocalize with pole-plasm markers, such as Stau (H). In UAS-osk flies, Dynamitin:GFP (J) and Stau (K) are mislocalized to the ectopic site in the middle of the oocyte. |
PMC1885955_fig5_11423.jpg | What is shown in this image? | The High-Level Overexpression of Centriole-Replication Proteins Drives the De Novo Formation of Centriole-like Structures in Unfertilized Eggs(A) Unfertilized eggs laid by WT, Ubq-GFP-DSas-6, Ubq-DSas-4-GFP, and Ubq-GFP-Sak females showing the distribution of endogenous DSas-4 (red) and MTs (green). The expression of GFP-DSas-6 can induce the formation of a relatively small number of centriole-like structures. The MT structures in the other eggs are the MTs that surround the polar bodies.(B) Unfertilized eggs laid by WT, UAS-GFP-DSas-6, UAS-DSas-4-GFP, and UAS-Sak-GFP females. All of the eggs are filled with many centriole-like structures.(C and D) Higher-magnification views of the centriole-like structures formed in eggs laid by UAS-GFP-DSas-6 (C), UAS-DSas-4-GFP (D), and UAS-Sak-GFP (E) females. GFP fluorescence is shown in the left panels (green in merged image), endogenous DSas-4 or D-PLP in the middle panels (blue in merged image), and MTs in the right panels (red in merged image).Scale bars represent 25 μm in (A) and (B) and 5 μm in (C)–(E). |
PMC1885955_fig5_11430.jpg | What is the central feature of this picture? | The High-Level Overexpression of Centriole-Replication Proteins Drives the De Novo Formation of Centriole-like Structures in Unfertilized Eggs(A) Unfertilized eggs laid by WT, Ubq-GFP-DSas-6, Ubq-DSas-4-GFP, and Ubq-GFP-Sak females showing the distribution of endogenous DSas-4 (red) and MTs (green). The expression of GFP-DSas-6 can induce the formation of a relatively small number of centriole-like structures. The MT structures in the other eggs are the MTs that surround the polar bodies.(B) Unfertilized eggs laid by WT, UAS-GFP-DSas-6, UAS-DSas-4-GFP, and UAS-Sak-GFP females. All of the eggs are filled with many centriole-like structures.(C and D) Higher-magnification views of the centriole-like structures formed in eggs laid by UAS-GFP-DSas-6 (C), UAS-DSas-4-GFP (D), and UAS-Sak-GFP (E) females. GFP fluorescence is shown in the left panels (green in merged image), endogenous DSas-4 or D-PLP in the middle panels (blue in merged image), and MTs in the right panels (red in merged image).Scale bars represent 25 μm in (A) and (B) and 5 μm in (C)–(E). |
PMC1885955_fig5_11419.jpg | What is the central feature of this picture? | The High-Level Overexpression of Centriole-Replication Proteins Drives the De Novo Formation of Centriole-like Structures in Unfertilized Eggs(A) Unfertilized eggs laid by WT, Ubq-GFP-DSas-6, Ubq-DSas-4-GFP, and Ubq-GFP-Sak females showing the distribution of endogenous DSas-4 (red) and MTs (green). The expression of GFP-DSas-6 can induce the formation of a relatively small number of centriole-like structures. The MT structures in the other eggs are the MTs that surround the polar bodies.(B) Unfertilized eggs laid by WT, UAS-GFP-DSas-6, UAS-DSas-4-GFP, and UAS-Sak-GFP females. All of the eggs are filled with many centriole-like structures.(C and D) Higher-magnification views of the centriole-like structures formed in eggs laid by UAS-GFP-DSas-6 (C), UAS-DSas-4-GFP (D), and UAS-Sak-GFP (E) females. GFP fluorescence is shown in the left panels (green in merged image), endogenous DSas-4 or D-PLP in the middle panels (blue in merged image), and MTs in the right panels (red in merged image).Scale bars represent 25 μm in (A) and (B) and 5 μm in (C)–(E). |
PMC1885955_fig5_11424.jpg | Describe the main subject of this image. | The High-Level Overexpression of Centriole-Replication Proteins Drives the De Novo Formation of Centriole-like Structures in Unfertilized Eggs(A) Unfertilized eggs laid by WT, Ubq-GFP-DSas-6, Ubq-DSas-4-GFP, and Ubq-GFP-Sak females showing the distribution of endogenous DSas-4 (red) and MTs (green). The expression of GFP-DSas-6 can induce the formation of a relatively small number of centriole-like structures. The MT structures in the other eggs are the MTs that surround the polar bodies.(B) Unfertilized eggs laid by WT, UAS-GFP-DSas-6, UAS-DSas-4-GFP, and UAS-Sak-GFP females. All of the eggs are filled with many centriole-like structures.(C and D) Higher-magnification views of the centriole-like structures formed in eggs laid by UAS-GFP-DSas-6 (C), UAS-DSas-4-GFP (D), and UAS-Sak-GFP (E) females. GFP fluorescence is shown in the left panels (green in merged image), endogenous DSas-4 or D-PLP in the middle panels (blue in merged image), and MTs in the right panels (red in merged image).Scale bars represent 25 μm in (A) and (B) and 5 μm in (C)–(E). |
PMC1885955_fig5_11422.jpg | What is the central feature of this picture? | The High-Level Overexpression of Centriole-Replication Proteins Drives the De Novo Formation of Centriole-like Structures in Unfertilized Eggs(A) Unfertilized eggs laid by WT, Ubq-GFP-DSas-6, Ubq-DSas-4-GFP, and Ubq-GFP-Sak females showing the distribution of endogenous DSas-4 (red) and MTs (green). The expression of GFP-DSas-6 can induce the formation of a relatively small number of centriole-like structures. The MT structures in the other eggs are the MTs that surround the polar bodies.(B) Unfertilized eggs laid by WT, UAS-GFP-DSas-6, UAS-DSas-4-GFP, and UAS-Sak-GFP females. All of the eggs are filled with many centriole-like structures.(C and D) Higher-magnification views of the centriole-like structures formed in eggs laid by UAS-GFP-DSas-6 (C), UAS-DSas-4-GFP (D), and UAS-Sak-GFP (E) females. GFP fluorescence is shown in the left panels (green in merged image), endogenous DSas-4 or D-PLP in the middle panels (blue in merged image), and MTs in the right panels (red in merged image).Scale bars represent 25 μm in (A) and (B) and 5 μm in (C)–(E). |
PMC1885955_fig5_11415.jpg | What is the focal point of this photograph? | The High-Level Overexpression of Centriole-Replication Proteins Drives the De Novo Formation of Centriole-like Structures in Unfertilized Eggs(A) Unfertilized eggs laid by WT, Ubq-GFP-DSas-6, Ubq-DSas-4-GFP, and Ubq-GFP-Sak females showing the distribution of endogenous DSas-4 (red) and MTs (green). The expression of GFP-DSas-6 can induce the formation of a relatively small number of centriole-like structures. The MT structures in the other eggs are the MTs that surround the polar bodies.(B) Unfertilized eggs laid by WT, UAS-GFP-DSas-6, UAS-DSas-4-GFP, and UAS-Sak-GFP females. All of the eggs are filled with many centriole-like structures.(C and D) Higher-magnification views of the centriole-like structures formed in eggs laid by UAS-GFP-DSas-6 (C), UAS-DSas-4-GFP (D), and UAS-Sak-GFP (E) females. GFP fluorescence is shown in the left panels (green in merged image), endogenous DSas-4 or D-PLP in the middle panels (blue in merged image), and MTs in the right panels (red in merged image).Scale bars represent 25 μm in (A) and (B) and 5 μm in (C)–(E). |
PMC1885955_fig5_11425.jpg | What can you see in this picture? | The High-Level Overexpression of Centriole-Replication Proteins Drives the De Novo Formation of Centriole-like Structures in Unfertilized Eggs(A) Unfertilized eggs laid by WT, Ubq-GFP-DSas-6, Ubq-DSas-4-GFP, and Ubq-GFP-Sak females showing the distribution of endogenous DSas-4 (red) and MTs (green). The expression of GFP-DSas-6 can induce the formation of a relatively small number of centriole-like structures. The MT structures in the other eggs are the MTs that surround the polar bodies.(B) Unfertilized eggs laid by WT, UAS-GFP-DSas-6, UAS-DSas-4-GFP, and UAS-Sak-GFP females. All of the eggs are filled with many centriole-like structures.(C and D) Higher-magnification views of the centriole-like structures formed in eggs laid by UAS-GFP-DSas-6 (C), UAS-DSas-4-GFP (D), and UAS-Sak-GFP (E) females. GFP fluorescence is shown in the left panels (green in merged image), endogenous DSas-4 or D-PLP in the middle panels (blue in merged image), and MTs in the right panels (red in merged image).Scale bars represent 25 μm in (A) and (B) and 5 μm in (C)–(E). |
PMC1885955_fig5_11426.jpg | Can you identify the primary element in this image? | The High-Level Overexpression of Centriole-Replication Proteins Drives the De Novo Formation of Centriole-like Structures in Unfertilized Eggs(A) Unfertilized eggs laid by WT, Ubq-GFP-DSas-6, Ubq-DSas-4-GFP, and Ubq-GFP-Sak females showing the distribution of endogenous DSas-4 (red) and MTs (green). The expression of GFP-DSas-6 can induce the formation of a relatively small number of centriole-like structures. The MT structures in the other eggs are the MTs that surround the polar bodies.(B) Unfertilized eggs laid by WT, UAS-GFP-DSas-6, UAS-DSas-4-GFP, and UAS-Sak-GFP females. All of the eggs are filled with many centriole-like structures.(C and D) Higher-magnification views of the centriole-like structures formed in eggs laid by UAS-GFP-DSas-6 (C), UAS-DSas-4-GFP (D), and UAS-Sak-GFP (E) females. GFP fluorescence is shown in the left panels (green in merged image), endogenous DSas-4 or D-PLP in the middle panels (blue in merged image), and MTs in the right panels (red in merged image).Scale bars represent 25 μm in (A) and (B) and 5 μm in (C)–(E). |
PMC1885955_fig5_11418.jpg | What is shown in this image? | The High-Level Overexpression of Centriole-Replication Proteins Drives the De Novo Formation of Centriole-like Structures in Unfertilized Eggs(A) Unfertilized eggs laid by WT, Ubq-GFP-DSas-6, Ubq-DSas-4-GFP, and Ubq-GFP-Sak females showing the distribution of endogenous DSas-4 (red) and MTs (green). The expression of GFP-DSas-6 can induce the formation of a relatively small number of centriole-like structures. The MT structures in the other eggs are the MTs that surround the polar bodies.(B) Unfertilized eggs laid by WT, UAS-GFP-DSas-6, UAS-DSas-4-GFP, and UAS-Sak-GFP females. All of the eggs are filled with many centriole-like structures.(C and D) Higher-magnification views of the centriole-like structures formed in eggs laid by UAS-GFP-DSas-6 (C), UAS-DSas-4-GFP (D), and UAS-Sak-GFP (E) females. GFP fluorescence is shown in the left panels (green in merged image), endogenous DSas-4 or D-PLP in the middle panels (blue in merged image), and MTs in the right panels (red in merged image).Scale bars represent 25 μm in (A) and (B) and 5 μm in (C)–(E). |
PMC1885955_fig5_11420.jpg | What is the central feature of this picture? | The High-Level Overexpression of Centriole-Replication Proteins Drives the De Novo Formation of Centriole-like Structures in Unfertilized Eggs(A) Unfertilized eggs laid by WT, Ubq-GFP-DSas-6, Ubq-DSas-4-GFP, and Ubq-GFP-Sak females showing the distribution of endogenous DSas-4 (red) and MTs (green). The expression of GFP-DSas-6 can induce the formation of a relatively small number of centriole-like structures. The MT structures in the other eggs are the MTs that surround the polar bodies.(B) Unfertilized eggs laid by WT, UAS-GFP-DSas-6, UAS-DSas-4-GFP, and UAS-Sak-GFP females. All of the eggs are filled with many centriole-like structures.(C and D) Higher-magnification views of the centriole-like structures formed in eggs laid by UAS-GFP-DSas-6 (C), UAS-DSas-4-GFP (D), and UAS-Sak-GFP (E) females. GFP fluorescence is shown in the left panels (green in merged image), endogenous DSas-4 or D-PLP in the middle panels (blue in merged image), and MTs in the right panels (red in merged image).Scale bars represent 25 μm in (A) and (B) and 5 μm in (C)–(E). |
PMC1885955_fig5_11428.jpg | What key item or scene is captured in this photo? | The High-Level Overexpression of Centriole-Replication Proteins Drives the De Novo Formation of Centriole-like Structures in Unfertilized Eggs(A) Unfertilized eggs laid by WT, Ubq-GFP-DSas-6, Ubq-DSas-4-GFP, and Ubq-GFP-Sak females showing the distribution of endogenous DSas-4 (red) and MTs (green). The expression of GFP-DSas-6 can induce the formation of a relatively small number of centriole-like structures. The MT structures in the other eggs are the MTs that surround the polar bodies.(B) Unfertilized eggs laid by WT, UAS-GFP-DSas-6, UAS-DSas-4-GFP, and UAS-Sak-GFP females. All of the eggs are filled with many centriole-like structures.(C and D) Higher-magnification views of the centriole-like structures formed in eggs laid by UAS-GFP-DSas-6 (C), UAS-DSas-4-GFP (D), and UAS-Sak-GFP (E) females. GFP fluorescence is shown in the left panels (green in merged image), endogenous DSas-4 or D-PLP in the middle panels (blue in merged image), and MTs in the right panels (red in merged image).Scale bars represent 25 μm in (A) and (B) and 5 μm in (C)–(E). |
PMC1885955_fig5_11432.jpg | What is the principal component of this image? | The High-Level Overexpression of Centriole-Replication Proteins Drives the De Novo Formation of Centriole-like Structures in Unfertilized Eggs(A) Unfertilized eggs laid by WT, Ubq-GFP-DSas-6, Ubq-DSas-4-GFP, and Ubq-GFP-Sak females showing the distribution of endogenous DSas-4 (red) and MTs (green). The expression of GFP-DSas-6 can induce the formation of a relatively small number of centriole-like structures. The MT structures in the other eggs are the MTs that surround the polar bodies.(B) Unfertilized eggs laid by WT, UAS-GFP-DSas-6, UAS-DSas-4-GFP, and UAS-Sak-GFP females. All of the eggs are filled with many centriole-like structures.(C and D) Higher-magnification views of the centriole-like structures formed in eggs laid by UAS-GFP-DSas-6 (C), UAS-DSas-4-GFP (D), and UAS-Sak-GFP (E) females. GFP fluorescence is shown in the left panels (green in merged image), endogenous DSas-4 or D-PLP in the middle panels (blue in merged image), and MTs in the right panels (red in merged image).Scale bars represent 25 μm in (A) and (B) and 5 μm in (C)–(E). |
PMC1885955_fig5_11414.jpg | What stands out most in this visual? | The High-Level Overexpression of Centriole-Replication Proteins Drives the De Novo Formation of Centriole-like Structures in Unfertilized Eggs(A) Unfertilized eggs laid by WT, Ubq-GFP-DSas-6, Ubq-DSas-4-GFP, and Ubq-GFP-Sak females showing the distribution of endogenous DSas-4 (red) and MTs (green). The expression of GFP-DSas-6 can induce the formation of a relatively small number of centriole-like structures. The MT structures in the other eggs are the MTs that surround the polar bodies.(B) Unfertilized eggs laid by WT, UAS-GFP-DSas-6, UAS-DSas-4-GFP, and UAS-Sak-GFP females. All of the eggs are filled with many centriole-like structures.(C and D) Higher-magnification views of the centriole-like structures formed in eggs laid by UAS-GFP-DSas-6 (C), UAS-DSas-4-GFP (D), and UAS-Sak-GFP (E) females. GFP fluorescence is shown in the left panels (green in merged image), endogenous DSas-4 or D-PLP in the middle panels (blue in merged image), and MTs in the right panels (red in merged image).Scale bars represent 25 μm in (A) and (B) and 5 μm in (C)–(E). |
PMC1885955_fig5_11413.jpg | What is the focal point of this photograph? | The High-Level Overexpression of Centriole-Replication Proteins Drives the De Novo Formation of Centriole-like Structures in Unfertilized Eggs(A) Unfertilized eggs laid by WT, Ubq-GFP-DSas-6, Ubq-DSas-4-GFP, and Ubq-GFP-Sak females showing the distribution of endogenous DSas-4 (red) and MTs (green). The expression of GFP-DSas-6 can induce the formation of a relatively small number of centriole-like structures. The MT structures in the other eggs are the MTs that surround the polar bodies.(B) Unfertilized eggs laid by WT, UAS-GFP-DSas-6, UAS-DSas-4-GFP, and UAS-Sak-GFP females. All of the eggs are filled with many centriole-like structures.(C and D) Higher-magnification views of the centriole-like structures formed in eggs laid by UAS-GFP-DSas-6 (C), UAS-DSas-4-GFP (D), and UAS-Sak-GFP (E) females. GFP fluorescence is shown in the left panels (green in merged image), endogenous DSas-4 or D-PLP in the middle panels (blue in merged image), and MTs in the right panels (red in merged image).Scale bars represent 25 μm in (A) and (B) and 5 μm in (C)–(E). |
PMC1885955_fig5_11416.jpg | What key item or scene is captured in this photo? | The High-Level Overexpression of Centriole-Replication Proteins Drives the De Novo Formation of Centriole-like Structures in Unfertilized Eggs(A) Unfertilized eggs laid by WT, Ubq-GFP-DSas-6, Ubq-DSas-4-GFP, and Ubq-GFP-Sak females showing the distribution of endogenous DSas-4 (red) and MTs (green). The expression of GFP-DSas-6 can induce the formation of a relatively small number of centriole-like structures. The MT structures in the other eggs are the MTs that surround the polar bodies.(B) Unfertilized eggs laid by WT, UAS-GFP-DSas-6, UAS-DSas-4-GFP, and UAS-Sak-GFP females. All of the eggs are filled with many centriole-like structures.(C and D) Higher-magnification views of the centriole-like structures formed in eggs laid by UAS-GFP-DSas-6 (C), UAS-DSas-4-GFP (D), and UAS-Sak-GFP (E) females. GFP fluorescence is shown in the left panels (green in merged image), endogenous DSas-4 or D-PLP in the middle panels (blue in merged image), and MTs in the right panels (red in merged image).Scale bars represent 25 μm in (A) and (B) and 5 μm in (C)–(E). |
PMC1885956_fig7_11466.jpg | What is being portrayed in this visual content? | Absence of the Follicular Stem Cell Niche, Altered Number and Location of Melanocyte Stem Cells and Melanoblasts, and Increased Epidermal and Dermal Proliferation in the K14-Cre; Smof/f SkinSkin sections from control (A, C, E, F, M, O, and Q) mutant (B, D, G–L, N, P, and R–T) mice.(A and B) Sections were processed for autoradiography 2 hr after 3H-TdR injection to show rapidly cycling cells (black).(C and D) Keratin 15 (K15) immunostaining (brown). Control hair follicles (HF) display K15 staining (arrows) in the bulge niche (C). (D) A mutant HF showing K15-positive cells abnormally located near the follicular matrix (arrow).(E–N) Sections processed for autoradiography 60 days after 3H-TdR injections to visualize label retaining cells (LRC; black). LRC representing HF stem cells (arrows) are nested in the bulge region of anagen (E) and telogen (F) control HF. Hair matrix of a pigmented HF at anagen (arrowhead in [F]). (G–L) The mutant follicles are devoid of a well-defined bulge niche with LRC. (G) A cyst wall (Cy) with a LRC (arrow). Inset in (G) is a low-magnification view. The mutant follicles contain LRC in their matrix (arrows in [H]) and in their associated dermal condensates and dermal papillae (arrowheads in [H]–[K]). (K) is a high-magnification view of the area indicated in (J). (L) Numerous stromal LRC (arrows) in the dermis of mutants. LRC (arrows) in control (M) and mutant (N) epidermises.(O–T) Bright-field images of sections hybridized with a Dct probe (the signal appears as black grains). Melanocyte stem cells in the bulge/sub-bulge (arrowheads in [Q]) and their amplifying progeny in the matrix (arrowheads in [O]) of control follicles. The mutant follicles show reduced numbers of Dct-positive cells (arrowheads in [P], [R], and [S]). Ectopic Dct-positive cells in the dermis of mutants (arrows in [R] and [T]). (Q) and (R) are high-magnification views of the areas indicated in (O) and (P), respectively. Inset in (S) is a low-magnification view.Scale bars: 50 μm (C–I, K, M, N, S, and T), 100 μm (A, B, J, L, Q, and R) and 200 μm (O and P). |
PMC1885956_fig7_11465.jpg | What is the central feature of this picture? | Absence of the Follicular Stem Cell Niche, Altered Number and Location of Melanocyte Stem Cells and Melanoblasts, and Increased Epidermal and Dermal Proliferation in the K14-Cre; Smof/f SkinSkin sections from control (A, C, E, F, M, O, and Q) mutant (B, D, G–L, N, P, and R–T) mice.(A and B) Sections were processed for autoradiography 2 hr after 3H-TdR injection to show rapidly cycling cells (black).(C and D) Keratin 15 (K15) immunostaining (brown). Control hair follicles (HF) display K15 staining (arrows) in the bulge niche (C). (D) A mutant HF showing K15-positive cells abnormally located near the follicular matrix (arrow).(E–N) Sections processed for autoradiography 60 days after 3H-TdR injections to visualize label retaining cells (LRC; black). LRC representing HF stem cells (arrows) are nested in the bulge region of anagen (E) and telogen (F) control HF. Hair matrix of a pigmented HF at anagen (arrowhead in [F]). (G–L) The mutant follicles are devoid of a well-defined bulge niche with LRC. (G) A cyst wall (Cy) with a LRC (arrow). Inset in (G) is a low-magnification view. The mutant follicles contain LRC in their matrix (arrows in [H]) and in their associated dermal condensates and dermal papillae (arrowheads in [H]–[K]). (K) is a high-magnification view of the area indicated in (J). (L) Numerous stromal LRC (arrows) in the dermis of mutants. LRC (arrows) in control (M) and mutant (N) epidermises.(O–T) Bright-field images of sections hybridized with a Dct probe (the signal appears as black grains). Melanocyte stem cells in the bulge/sub-bulge (arrowheads in [Q]) and their amplifying progeny in the matrix (arrowheads in [O]) of control follicles. The mutant follicles show reduced numbers of Dct-positive cells (arrowheads in [P], [R], and [S]). Ectopic Dct-positive cells in the dermis of mutants (arrows in [R] and [T]). (Q) and (R) are high-magnification views of the areas indicated in (O) and (P), respectively. Inset in (S) is a low-magnification view.Scale bars: 50 μm (C–I, K, M, N, S, and T), 100 μm (A, B, J, L, Q, and R) and 200 μm (O and P). |
PMC1885956_fig7_11450.jpg | What stands out most in this visual? | Absence of the Follicular Stem Cell Niche, Altered Number and Location of Melanocyte Stem Cells and Melanoblasts, and Increased Epidermal and Dermal Proliferation in the K14-Cre; Smof/f SkinSkin sections from control (A, C, E, F, M, O, and Q) mutant (B, D, G–L, N, P, and R–T) mice.(A and B) Sections were processed for autoradiography 2 hr after 3H-TdR injection to show rapidly cycling cells (black).(C and D) Keratin 15 (K15) immunostaining (brown). Control hair follicles (HF) display K15 staining (arrows) in the bulge niche (C). (D) A mutant HF showing K15-positive cells abnormally located near the follicular matrix (arrow).(E–N) Sections processed for autoradiography 60 days after 3H-TdR injections to visualize label retaining cells (LRC; black). LRC representing HF stem cells (arrows) are nested in the bulge region of anagen (E) and telogen (F) control HF. Hair matrix of a pigmented HF at anagen (arrowhead in [F]). (G–L) The mutant follicles are devoid of a well-defined bulge niche with LRC. (G) A cyst wall (Cy) with a LRC (arrow). Inset in (G) is a low-magnification view. The mutant follicles contain LRC in their matrix (arrows in [H]) and in their associated dermal condensates and dermal papillae (arrowheads in [H]–[K]). (K) is a high-magnification view of the area indicated in (J). (L) Numerous stromal LRC (arrows) in the dermis of mutants. LRC (arrows) in control (M) and mutant (N) epidermises.(O–T) Bright-field images of sections hybridized with a Dct probe (the signal appears as black grains). Melanocyte stem cells in the bulge/sub-bulge (arrowheads in [Q]) and their amplifying progeny in the matrix (arrowheads in [O]) of control follicles. The mutant follicles show reduced numbers of Dct-positive cells (arrowheads in [P], [R], and [S]). Ectopic Dct-positive cells in the dermis of mutants (arrows in [R] and [T]). (Q) and (R) are high-magnification views of the areas indicated in (O) and (P), respectively. Inset in (S) is a low-magnification view.Scale bars: 50 μm (C–I, K, M, N, S, and T), 100 μm (A, B, J, L, Q, and R) and 200 μm (O and P). |
PMC1885956_fig7_11457.jpg | What is the central feature of this picture? | Absence of the Follicular Stem Cell Niche, Altered Number and Location of Melanocyte Stem Cells and Melanoblasts, and Increased Epidermal and Dermal Proliferation in the K14-Cre; Smof/f SkinSkin sections from control (A, C, E, F, M, O, and Q) mutant (B, D, G–L, N, P, and R–T) mice.(A and B) Sections were processed for autoradiography 2 hr after 3H-TdR injection to show rapidly cycling cells (black).(C and D) Keratin 15 (K15) immunostaining (brown). Control hair follicles (HF) display K15 staining (arrows) in the bulge niche (C). (D) A mutant HF showing K15-positive cells abnormally located near the follicular matrix (arrow).(E–N) Sections processed for autoradiography 60 days after 3H-TdR injections to visualize label retaining cells (LRC; black). LRC representing HF stem cells (arrows) are nested in the bulge region of anagen (E) and telogen (F) control HF. Hair matrix of a pigmented HF at anagen (arrowhead in [F]). (G–L) The mutant follicles are devoid of a well-defined bulge niche with LRC. (G) A cyst wall (Cy) with a LRC (arrow). Inset in (G) is a low-magnification view. The mutant follicles contain LRC in their matrix (arrows in [H]) and in their associated dermal condensates and dermal papillae (arrowheads in [H]–[K]). (K) is a high-magnification view of the area indicated in (J). (L) Numerous stromal LRC (arrows) in the dermis of mutants. LRC (arrows) in control (M) and mutant (N) epidermises.(O–T) Bright-field images of sections hybridized with a Dct probe (the signal appears as black grains). Melanocyte stem cells in the bulge/sub-bulge (arrowheads in [Q]) and their amplifying progeny in the matrix (arrowheads in [O]) of control follicles. The mutant follicles show reduced numbers of Dct-positive cells (arrowheads in [P], [R], and [S]). Ectopic Dct-positive cells in the dermis of mutants (arrows in [R] and [T]). (Q) and (R) are high-magnification views of the areas indicated in (O) and (P), respectively. Inset in (S) is a low-magnification view.Scale bars: 50 μm (C–I, K, M, N, S, and T), 100 μm (A, B, J, L, Q, and R) and 200 μm (O and P). |
PMC1885956_fig7_11459.jpg | What is shown in this image? | Absence of the Follicular Stem Cell Niche, Altered Number and Location of Melanocyte Stem Cells and Melanoblasts, and Increased Epidermal and Dermal Proliferation in the K14-Cre; Smof/f SkinSkin sections from control (A, C, E, F, M, O, and Q) mutant (B, D, G–L, N, P, and R–T) mice.(A and B) Sections were processed for autoradiography 2 hr after 3H-TdR injection to show rapidly cycling cells (black).(C and D) Keratin 15 (K15) immunostaining (brown). Control hair follicles (HF) display K15 staining (arrows) in the bulge niche (C). (D) A mutant HF showing K15-positive cells abnormally located near the follicular matrix (arrow).(E–N) Sections processed for autoradiography 60 days after 3H-TdR injections to visualize label retaining cells (LRC; black). LRC representing HF stem cells (arrows) are nested in the bulge region of anagen (E) and telogen (F) control HF. Hair matrix of a pigmented HF at anagen (arrowhead in [F]). (G–L) The mutant follicles are devoid of a well-defined bulge niche with LRC. (G) A cyst wall (Cy) with a LRC (arrow). Inset in (G) is a low-magnification view. The mutant follicles contain LRC in their matrix (arrows in [H]) and in their associated dermal condensates and dermal papillae (arrowheads in [H]–[K]). (K) is a high-magnification view of the area indicated in (J). (L) Numerous stromal LRC (arrows) in the dermis of mutants. LRC (arrows) in control (M) and mutant (N) epidermises.(O–T) Bright-field images of sections hybridized with a Dct probe (the signal appears as black grains). Melanocyte stem cells in the bulge/sub-bulge (arrowheads in [Q]) and their amplifying progeny in the matrix (arrowheads in [O]) of control follicles. The mutant follicles show reduced numbers of Dct-positive cells (arrowheads in [P], [R], and [S]). Ectopic Dct-positive cells in the dermis of mutants (arrows in [R] and [T]). (Q) and (R) are high-magnification views of the areas indicated in (O) and (P), respectively. Inset in (S) is a low-magnification view.Scale bars: 50 μm (C–I, K, M, N, S, and T), 100 μm (A, B, J, L, Q, and R) and 200 μm (O and P). |
PMC1885956_fig7_11453.jpg | What is the dominant medical problem in this image? | Absence of the Follicular Stem Cell Niche, Altered Number and Location of Melanocyte Stem Cells and Melanoblasts, and Increased Epidermal and Dermal Proliferation in the K14-Cre; Smof/f SkinSkin sections from control (A, C, E, F, M, O, and Q) mutant (B, D, G–L, N, P, and R–T) mice.(A and B) Sections were processed for autoradiography 2 hr after 3H-TdR injection to show rapidly cycling cells (black).(C and D) Keratin 15 (K15) immunostaining (brown). Control hair follicles (HF) display K15 staining (arrows) in the bulge niche (C). (D) A mutant HF showing K15-positive cells abnormally located near the follicular matrix (arrow).(E–N) Sections processed for autoradiography 60 days after 3H-TdR injections to visualize label retaining cells (LRC; black). LRC representing HF stem cells (arrows) are nested in the bulge region of anagen (E) and telogen (F) control HF. Hair matrix of a pigmented HF at anagen (arrowhead in [F]). (G–L) The mutant follicles are devoid of a well-defined bulge niche with LRC. (G) A cyst wall (Cy) with a LRC (arrow). Inset in (G) is a low-magnification view. The mutant follicles contain LRC in their matrix (arrows in [H]) and in their associated dermal condensates and dermal papillae (arrowheads in [H]–[K]). (K) is a high-magnification view of the area indicated in (J). (L) Numerous stromal LRC (arrows) in the dermis of mutants. LRC (arrows) in control (M) and mutant (N) epidermises.(O–T) Bright-field images of sections hybridized with a Dct probe (the signal appears as black grains). Melanocyte stem cells in the bulge/sub-bulge (arrowheads in [Q]) and their amplifying progeny in the matrix (arrowheads in [O]) of control follicles. The mutant follicles show reduced numbers of Dct-positive cells (arrowheads in [P], [R], and [S]). Ectopic Dct-positive cells in the dermis of mutants (arrows in [R] and [T]). (Q) and (R) are high-magnification views of the areas indicated in (O) and (P), respectively. Inset in (S) is a low-magnification view.Scale bars: 50 μm (C–I, K, M, N, S, and T), 100 μm (A, B, J, L, Q, and R) and 200 μm (O and P). |
PMC1885956_fig7_11460.jpg | What object or scene is depicted here? | Absence of the Follicular Stem Cell Niche, Altered Number and Location of Melanocyte Stem Cells and Melanoblasts, and Increased Epidermal and Dermal Proliferation in the K14-Cre; Smof/f SkinSkin sections from control (A, C, E, F, M, O, and Q) mutant (B, D, G–L, N, P, and R–T) mice.(A and B) Sections were processed for autoradiography 2 hr after 3H-TdR injection to show rapidly cycling cells (black).(C and D) Keratin 15 (K15) immunostaining (brown). Control hair follicles (HF) display K15 staining (arrows) in the bulge niche (C). (D) A mutant HF showing K15-positive cells abnormally located near the follicular matrix (arrow).(E–N) Sections processed for autoradiography 60 days after 3H-TdR injections to visualize label retaining cells (LRC; black). LRC representing HF stem cells (arrows) are nested in the bulge region of anagen (E) and telogen (F) control HF. Hair matrix of a pigmented HF at anagen (arrowhead in [F]). (G–L) The mutant follicles are devoid of a well-defined bulge niche with LRC. (G) A cyst wall (Cy) with a LRC (arrow). Inset in (G) is a low-magnification view. The mutant follicles contain LRC in their matrix (arrows in [H]) and in their associated dermal condensates and dermal papillae (arrowheads in [H]–[K]). (K) is a high-magnification view of the area indicated in (J). (L) Numerous stromal LRC (arrows) in the dermis of mutants. LRC (arrows) in control (M) and mutant (N) epidermises.(O–T) Bright-field images of sections hybridized with a Dct probe (the signal appears as black grains). Melanocyte stem cells in the bulge/sub-bulge (arrowheads in [Q]) and their amplifying progeny in the matrix (arrowheads in [O]) of control follicles. The mutant follicles show reduced numbers of Dct-positive cells (arrowheads in [P], [R], and [S]). Ectopic Dct-positive cells in the dermis of mutants (arrows in [R] and [T]). (Q) and (R) are high-magnification views of the areas indicated in (O) and (P), respectively. Inset in (S) is a low-magnification view.Scale bars: 50 μm (C–I, K, M, N, S, and T), 100 μm (A, B, J, L, Q, and R) and 200 μm (O and P). |
PMC1885956_fig7_11455.jpg | What is being portrayed in this visual content? | Absence of the Follicular Stem Cell Niche, Altered Number and Location of Melanocyte Stem Cells and Melanoblasts, and Increased Epidermal and Dermal Proliferation in the K14-Cre; Smof/f SkinSkin sections from control (A, C, E, F, M, O, and Q) mutant (B, D, G–L, N, P, and R–T) mice.(A and B) Sections were processed for autoradiography 2 hr after 3H-TdR injection to show rapidly cycling cells (black).(C and D) Keratin 15 (K15) immunostaining (brown). Control hair follicles (HF) display K15 staining (arrows) in the bulge niche (C). (D) A mutant HF showing K15-positive cells abnormally located near the follicular matrix (arrow).(E–N) Sections processed for autoradiography 60 days after 3H-TdR injections to visualize label retaining cells (LRC; black). LRC representing HF stem cells (arrows) are nested in the bulge region of anagen (E) and telogen (F) control HF. Hair matrix of a pigmented HF at anagen (arrowhead in [F]). (G–L) The mutant follicles are devoid of a well-defined bulge niche with LRC. (G) A cyst wall (Cy) with a LRC (arrow). Inset in (G) is a low-magnification view. The mutant follicles contain LRC in their matrix (arrows in [H]) and in their associated dermal condensates and dermal papillae (arrowheads in [H]–[K]). (K) is a high-magnification view of the area indicated in (J). (L) Numerous stromal LRC (arrows) in the dermis of mutants. LRC (arrows) in control (M) and mutant (N) epidermises.(O–T) Bright-field images of sections hybridized with a Dct probe (the signal appears as black grains). Melanocyte stem cells in the bulge/sub-bulge (arrowheads in [Q]) and their amplifying progeny in the matrix (arrowheads in [O]) of control follicles. The mutant follicles show reduced numbers of Dct-positive cells (arrowheads in [P], [R], and [S]). Ectopic Dct-positive cells in the dermis of mutants (arrows in [R] and [T]). (Q) and (R) are high-magnification views of the areas indicated in (O) and (P), respectively. Inset in (S) is a low-magnification view.Scale bars: 50 μm (C–I, K, M, N, S, and T), 100 μm (A, B, J, L, Q, and R) and 200 μm (O and P). |
PMC1885956_fig7_11461.jpg | What key item or scene is captured in this photo? | Absence of the Follicular Stem Cell Niche, Altered Number and Location of Melanocyte Stem Cells and Melanoblasts, and Increased Epidermal and Dermal Proliferation in the K14-Cre; Smof/f SkinSkin sections from control (A, C, E, F, M, O, and Q) mutant (B, D, G–L, N, P, and R–T) mice.(A and B) Sections were processed for autoradiography 2 hr after 3H-TdR injection to show rapidly cycling cells (black).(C and D) Keratin 15 (K15) immunostaining (brown). Control hair follicles (HF) display K15 staining (arrows) in the bulge niche (C). (D) A mutant HF showing K15-positive cells abnormally located near the follicular matrix (arrow).(E–N) Sections processed for autoradiography 60 days after 3H-TdR injections to visualize label retaining cells (LRC; black). LRC representing HF stem cells (arrows) are nested in the bulge region of anagen (E) and telogen (F) control HF. Hair matrix of a pigmented HF at anagen (arrowhead in [F]). (G–L) The mutant follicles are devoid of a well-defined bulge niche with LRC. (G) A cyst wall (Cy) with a LRC (arrow). Inset in (G) is a low-magnification view. The mutant follicles contain LRC in their matrix (arrows in [H]) and in their associated dermal condensates and dermal papillae (arrowheads in [H]–[K]). (K) is a high-magnification view of the area indicated in (J). (L) Numerous stromal LRC (arrows) in the dermis of mutants. LRC (arrows) in control (M) and mutant (N) epidermises.(O–T) Bright-field images of sections hybridized with a Dct probe (the signal appears as black grains). Melanocyte stem cells in the bulge/sub-bulge (arrowheads in [Q]) and their amplifying progeny in the matrix (arrowheads in [O]) of control follicles. The mutant follicles show reduced numbers of Dct-positive cells (arrowheads in [P], [R], and [S]). Ectopic Dct-positive cells in the dermis of mutants (arrows in [R] and [T]). (Q) and (R) are high-magnification views of the areas indicated in (O) and (P), respectively. Inset in (S) is a low-magnification view.Scale bars: 50 μm (C–I, K, M, N, S, and T), 100 μm (A, B, J, L, Q, and R) and 200 μm (O and P). |
PMC1885956_fig7_11451.jpg | What is the core subject represented in this visual? | Absence of the Follicular Stem Cell Niche, Altered Number and Location of Melanocyte Stem Cells and Melanoblasts, and Increased Epidermal and Dermal Proliferation in the K14-Cre; Smof/f SkinSkin sections from control (A, C, E, F, M, O, and Q) mutant (B, D, G–L, N, P, and R–T) mice.(A and B) Sections were processed for autoradiography 2 hr after 3H-TdR injection to show rapidly cycling cells (black).(C and D) Keratin 15 (K15) immunostaining (brown). Control hair follicles (HF) display K15 staining (arrows) in the bulge niche (C). (D) A mutant HF showing K15-positive cells abnormally located near the follicular matrix (arrow).(E–N) Sections processed for autoradiography 60 days after 3H-TdR injections to visualize label retaining cells (LRC; black). LRC representing HF stem cells (arrows) are nested in the bulge region of anagen (E) and telogen (F) control HF. Hair matrix of a pigmented HF at anagen (arrowhead in [F]). (G–L) The mutant follicles are devoid of a well-defined bulge niche with LRC. (G) A cyst wall (Cy) with a LRC (arrow). Inset in (G) is a low-magnification view. The mutant follicles contain LRC in their matrix (arrows in [H]) and in their associated dermal condensates and dermal papillae (arrowheads in [H]–[K]). (K) is a high-magnification view of the area indicated in (J). (L) Numerous stromal LRC (arrows) in the dermis of mutants. LRC (arrows) in control (M) and mutant (N) epidermises.(O–T) Bright-field images of sections hybridized with a Dct probe (the signal appears as black grains). Melanocyte stem cells in the bulge/sub-bulge (arrowheads in [Q]) and their amplifying progeny in the matrix (arrowheads in [O]) of control follicles. The mutant follicles show reduced numbers of Dct-positive cells (arrowheads in [P], [R], and [S]). Ectopic Dct-positive cells in the dermis of mutants (arrows in [R] and [T]). (Q) and (R) are high-magnification views of the areas indicated in (O) and (P), respectively. Inset in (S) is a low-magnification view.Scale bars: 50 μm (C–I, K, M, N, S, and T), 100 μm (A, B, J, L, Q, and R) and 200 μm (O and P). |
PMC1885956_fig7_11452.jpg | Can you identify the primary element in this image? | Absence of the Follicular Stem Cell Niche, Altered Number and Location of Melanocyte Stem Cells and Melanoblasts, and Increased Epidermal and Dermal Proliferation in the K14-Cre; Smof/f SkinSkin sections from control (A, C, E, F, M, O, and Q) mutant (B, D, G–L, N, P, and R–T) mice.(A and B) Sections were processed for autoradiography 2 hr after 3H-TdR injection to show rapidly cycling cells (black).(C and D) Keratin 15 (K15) immunostaining (brown). Control hair follicles (HF) display K15 staining (arrows) in the bulge niche (C). (D) A mutant HF showing K15-positive cells abnormally located near the follicular matrix (arrow).(E–N) Sections processed for autoradiography 60 days after 3H-TdR injections to visualize label retaining cells (LRC; black). LRC representing HF stem cells (arrows) are nested in the bulge region of anagen (E) and telogen (F) control HF. Hair matrix of a pigmented HF at anagen (arrowhead in [F]). (G–L) The mutant follicles are devoid of a well-defined bulge niche with LRC. (G) A cyst wall (Cy) with a LRC (arrow). Inset in (G) is a low-magnification view. The mutant follicles contain LRC in their matrix (arrows in [H]) and in their associated dermal condensates and dermal papillae (arrowheads in [H]–[K]). (K) is a high-magnification view of the area indicated in (J). (L) Numerous stromal LRC (arrows) in the dermis of mutants. LRC (arrows) in control (M) and mutant (N) epidermises.(O–T) Bright-field images of sections hybridized with a Dct probe (the signal appears as black grains). Melanocyte stem cells in the bulge/sub-bulge (arrowheads in [Q]) and their amplifying progeny in the matrix (arrowheads in [O]) of control follicles. The mutant follicles show reduced numbers of Dct-positive cells (arrowheads in [P], [R], and [S]). Ectopic Dct-positive cells in the dermis of mutants (arrows in [R] and [T]). (Q) and (R) are high-magnification views of the areas indicated in (O) and (P), respectively. Inset in (S) is a low-magnification view.Scale bars: 50 μm (C–I, K, M, N, S, and T), 100 μm (A, B, J, L, Q, and R) and 200 μm (O and P). |
PMC1885956_fig7_11467.jpg | What is being portrayed in this visual content? | Absence of the Follicular Stem Cell Niche, Altered Number and Location of Melanocyte Stem Cells and Melanoblasts, and Increased Epidermal and Dermal Proliferation in the K14-Cre; Smof/f SkinSkin sections from control (A, C, E, F, M, O, and Q) mutant (B, D, G–L, N, P, and R–T) mice.(A and B) Sections were processed for autoradiography 2 hr after 3H-TdR injection to show rapidly cycling cells (black).(C and D) Keratin 15 (K15) immunostaining (brown). Control hair follicles (HF) display K15 staining (arrows) in the bulge niche (C). (D) A mutant HF showing K15-positive cells abnormally located near the follicular matrix (arrow).(E–N) Sections processed for autoradiography 60 days after 3H-TdR injections to visualize label retaining cells (LRC; black). LRC representing HF stem cells (arrows) are nested in the bulge region of anagen (E) and telogen (F) control HF. Hair matrix of a pigmented HF at anagen (arrowhead in [F]). (G–L) The mutant follicles are devoid of a well-defined bulge niche with LRC. (G) A cyst wall (Cy) with a LRC (arrow). Inset in (G) is a low-magnification view. The mutant follicles contain LRC in their matrix (arrows in [H]) and in their associated dermal condensates and dermal papillae (arrowheads in [H]–[K]). (K) is a high-magnification view of the area indicated in (J). (L) Numerous stromal LRC (arrows) in the dermis of mutants. LRC (arrows) in control (M) and mutant (N) epidermises.(O–T) Bright-field images of sections hybridized with a Dct probe (the signal appears as black grains). Melanocyte stem cells in the bulge/sub-bulge (arrowheads in [Q]) and their amplifying progeny in the matrix (arrowheads in [O]) of control follicles. The mutant follicles show reduced numbers of Dct-positive cells (arrowheads in [P], [R], and [S]). Ectopic Dct-positive cells in the dermis of mutants (arrows in [R] and [T]). (Q) and (R) are high-magnification views of the areas indicated in (O) and (P), respectively. Inset in (S) is a low-magnification view.Scale bars: 50 μm (C–I, K, M, N, S, and T), 100 μm (A, B, J, L, Q, and R) and 200 μm (O and P). |
PMC1885956_fig7_11458.jpg | What can you see in this picture? | Absence of the Follicular Stem Cell Niche, Altered Number and Location of Melanocyte Stem Cells and Melanoblasts, and Increased Epidermal and Dermal Proliferation in the K14-Cre; Smof/f SkinSkin sections from control (A, C, E, F, M, O, and Q) mutant (B, D, G–L, N, P, and R–T) mice.(A and B) Sections were processed for autoradiography 2 hr after 3H-TdR injection to show rapidly cycling cells (black).(C and D) Keratin 15 (K15) immunostaining (brown). Control hair follicles (HF) display K15 staining (arrows) in the bulge niche (C). (D) A mutant HF showing K15-positive cells abnormally located near the follicular matrix (arrow).(E–N) Sections processed for autoradiography 60 days after 3H-TdR injections to visualize label retaining cells (LRC; black). LRC representing HF stem cells (arrows) are nested in the bulge region of anagen (E) and telogen (F) control HF. Hair matrix of a pigmented HF at anagen (arrowhead in [F]). (G–L) The mutant follicles are devoid of a well-defined bulge niche with LRC. (G) A cyst wall (Cy) with a LRC (arrow). Inset in (G) is a low-magnification view. The mutant follicles contain LRC in their matrix (arrows in [H]) and in their associated dermal condensates and dermal papillae (arrowheads in [H]–[K]). (K) is a high-magnification view of the area indicated in (J). (L) Numerous stromal LRC (arrows) in the dermis of mutants. LRC (arrows) in control (M) and mutant (N) epidermises.(O–T) Bright-field images of sections hybridized with a Dct probe (the signal appears as black grains). Melanocyte stem cells in the bulge/sub-bulge (arrowheads in [Q]) and their amplifying progeny in the matrix (arrowheads in [O]) of control follicles. The mutant follicles show reduced numbers of Dct-positive cells (arrowheads in [P], [R], and [S]). Ectopic Dct-positive cells in the dermis of mutants (arrows in [R] and [T]). (Q) and (R) are high-magnification views of the areas indicated in (O) and (P), respectively. Inset in (S) is a low-magnification view.Scale bars: 50 μm (C–I, K, M, N, S, and T), 100 μm (A, B, J, L, Q, and R) and 200 μm (O and P). |
PMC1885956_fig7_11464.jpg | What is shown in this image? | Absence of the Follicular Stem Cell Niche, Altered Number and Location of Melanocyte Stem Cells and Melanoblasts, and Increased Epidermal and Dermal Proliferation in the K14-Cre; Smof/f SkinSkin sections from control (A, C, E, F, M, O, and Q) mutant (B, D, G–L, N, P, and R–T) mice.(A and B) Sections were processed for autoradiography 2 hr after 3H-TdR injection to show rapidly cycling cells (black).(C and D) Keratin 15 (K15) immunostaining (brown). Control hair follicles (HF) display K15 staining (arrows) in the bulge niche (C). (D) A mutant HF showing K15-positive cells abnormally located near the follicular matrix (arrow).(E–N) Sections processed for autoradiography 60 days after 3H-TdR injections to visualize label retaining cells (LRC; black). LRC representing HF stem cells (arrows) are nested in the bulge region of anagen (E) and telogen (F) control HF. Hair matrix of a pigmented HF at anagen (arrowhead in [F]). (G–L) The mutant follicles are devoid of a well-defined bulge niche with LRC. (G) A cyst wall (Cy) with a LRC (arrow). Inset in (G) is a low-magnification view. The mutant follicles contain LRC in their matrix (arrows in [H]) and in their associated dermal condensates and dermal papillae (arrowheads in [H]–[K]). (K) is a high-magnification view of the area indicated in (J). (L) Numerous stromal LRC (arrows) in the dermis of mutants. LRC (arrows) in control (M) and mutant (N) epidermises.(O–T) Bright-field images of sections hybridized with a Dct probe (the signal appears as black grains). Melanocyte stem cells in the bulge/sub-bulge (arrowheads in [Q]) and their amplifying progeny in the matrix (arrowheads in [O]) of control follicles. The mutant follicles show reduced numbers of Dct-positive cells (arrowheads in [P], [R], and [S]). Ectopic Dct-positive cells in the dermis of mutants (arrows in [R] and [T]). (Q) and (R) are high-magnification views of the areas indicated in (O) and (P), respectively. Inset in (S) is a low-magnification view.Scale bars: 50 μm (C–I, K, M, N, S, and T), 100 μm (A, B, J, L, Q, and R) and 200 μm (O and P). |
PMC1885956_fig7_11454.jpg | What is the central feature of this picture? | Absence of the Follicular Stem Cell Niche, Altered Number and Location of Melanocyte Stem Cells and Melanoblasts, and Increased Epidermal and Dermal Proliferation in the K14-Cre; Smof/f SkinSkin sections from control (A, C, E, F, M, O, and Q) mutant (B, D, G–L, N, P, and R–T) mice.(A and B) Sections were processed for autoradiography 2 hr after 3H-TdR injection to show rapidly cycling cells (black).(C and D) Keratin 15 (K15) immunostaining (brown). Control hair follicles (HF) display K15 staining (arrows) in the bulge niche (C). (D) A mutant HF showing K15-positive cells abnormally located near the follicular matrix (arrow).(E–N) Sections processed for autoradiography 60 days after 3H-TdR injections to visualize label retaining cells (LRC; black). LRC representing HF stem cells (arrows) are nested in the bulge region of anagen (E) and telogen (F) control HF. Hair matrix of a pigmented HF at anagen (arrowhead in [F]). (G–L) The mutant follicles are devoid of a well-defined bulge niche with LRC. (G) A cyst wall (Cy) with a LRC (arrow). Inset in (G) is a low-magnification view. The mutant follicles contain LRC in their matrix (arrows in [H]) and in their associated dermal condensates and dermal papillae (arrowheads in [H]–[K]). (K) is a high-magnification view of the area indicated in (J). (L) Numerous stromal LRC (arrows) in the dermis of mutants. LRC (arrows) in control (M) and mutant (N) epidermises.(O–T) Bright-field images of sections hybridized with a Dct probe (the signal appears as black grains). Melanocyte stem cells in the bulge/sub-bulge (arrowheads in [Q]) and their amplifying progeny in the matrix (arrowheads in [O]) of control follicles. The mutant follicles show reduced numbers of Dct-positive cells (arrowheads in [P], [R], and [S]). Ectopic Dct-positive cells in the dermis of mutants (arrows in [R] and [T]). (Q) and (R) are high-magnification views of the areas indicated in (O) and (P), respectively. Inset in (S) is a low-magnification view.Scale bars: 50 μm (C–I, K, M, N, S, and T), 100 μm (A, B, J, L, Q, and R) and 200 μm (O and P). |
PMC1885958_fig1_11437.jpg | What can you see in this picture? | Separation of Vaginal Epithelial Sheets(A) Photograph of suction blisters on surgically excised vaginal mucosa.(B) Hematoxylin-eosin stain of intact suction blister by light microscopy.(C) Blister roofs, i.e., epithelial sheets, floating in PBS after removal from the underlying stroma, visualized under a stereoscope.(D) Epithelial sheets, separated by EDTA treatment.(E) Stereoscopic view of the basal side of a sheet separated by vacuum suction. An organized pattern of rete ridges and depressions, corresponding to the stromal papillae that were pulled out during separation, can be seen.(F) Stereoscopic view of the basal side of an EDTA-separated sheet, exhibiting the same pattern.(G and H) Toluidine blue-stained cross-section of epithelial sheets separated by vacuum suction (G) or ETDA (H), viewed by light microscopy. In the EDTA sheet, the enucleated outer epithelial cells have swollen during the overnight incubation.(I and J) Live/dead cell staining of EDTA-separated sheets. Sheets were stained with calcein AM (live cells, green), ethidium homodimer-1 (nuclei of dead cells, red), and TOPRO-3 (nuclear counterstain, blue) as described in the manufacturer's protocol. Sheets were immersed in glycerol under a coverslip and imaged by confocal microscopy. Stacks covering the complete distance from the basal to the luminal side (toward the vaginal cavity) were acquired, and the sheets were reconstructed in the z-section by Imaris software.(I) In a typical sheet, nearly all cells were alive, staining green, and only few cells at the luminal side were dead, staining red, which represent naturally dying cells that slough off into the vaginal cavity in vivo (two white arrows).(J) Treatment for 1 hr with 1% sodium azide killed all cells, as demonstrated by loss of the green live cell stain and universal acquisition of the red dead cell marker. |
PMC1885958_fig1_11436.jpg | What is the central feature of this picture? | Separation of Vaginal Epithelial Sheets(A) Photograph of suction blisters on surgically excised vaginal mucosa.(B) Hematoxylin-eosin stain of intact suction blister by light microscopy.(C) Blister roofs, i.e., epithelial sheets, floating in PBS after removal from the underlying stroma, visualized under a stereoscope.(D) Epithelial sheets, separated by EDTA treatment.(E) Stereoscopic view of the basal side of a sheet separated by vacuum suction. An organized pattern of rete ridges and depressions, corresponding to the stromal papillae that were pulled out during separation, can be seen.(F) Stereoscopic view of the basal side of an EDTA-separated sheet, exhibiting the same pattern.(G and H) Toluidine blue-stained cross-section of epithelial sheets separated by vacuum suction (G) or ETDA (H), viewed by light microscopy. In the EDTA sheet, the enucleated outer epithelial cells have swollen during the overnight incubation.(I and J) Live/dead cell staining of EDTA-separated sheets. Sheets were stained with calcein AM (live cells, green), ethidium homodimer-1 (nuclei of dead cells, red), and TOPRO-3 (nuclear counterstain, blue) as described in the manufacturer's protocol. Sheets were immersed in glycerol under a coverslip and imaged by confocal microscopy. Stacks covering the complete distance from the basal to the luminal side (toward the vaginal cavity) were acquired, and the sheets were reconstructed in the z-section by Imaris software.(I) In a typical sheet, nearly all cells were alive, staining green, and only few cells at the luminal side were dead, staining red, which represent naturally dying cells that slough off into the vaginal cavity in vivo (two white arrows).(J) Treatment for 1 hr with 1% sodium azide killed all cells, as demonstrated by loss of the green live cell stain and universal acquisition of the red dead cell marker. |
PMC1885958_fig1_11438.jpg | What is the central feature of this picture? | Separation of Vaginal Epithelial Sheets(A) Photograph of suction blisters on surgically excised vaginal mucosa.(B) Hematoxylin-eosin stain of intact suction blister by light microscopy.(C) Blister roofs, i.e., epithelial sheets, floating in PBS after removal from the underlying stroma, visualized under a stereoscope.(D) Epithelial sheets, separated by EDTA treatment.(E) Stereoscopic view of the basal side of a sheet separated by vacuum suction. An organized pattern of rete ridges and depressions, corresponding to the stromal papillae that were pulled out during separation, can be seen.(F) Stereoscopic view of the basal side of an EDTA-separated sheet, exhibiting the same pattern.(G and H) Toluidine blue-stained cross-section of epithelial sheets separated by vacuum suction (G) or ETDA (H), viewed by light microscopy. In the EDTA sheet, the enucleated outer epithelial cells have swollen during the overnight incubation.(I and J) Live/dead cell staining of EDTA-separated sheets. Sheets were stained with calcein AM (live cells, green), ethidium homodimer-1 (nuclei of dead cells, red), and TOPRO-3 (nuclear counterstain, blue) as described in the manufacturer's protocol. Sheets were immersed in glycerol under a coverslip and imaged by confocal microscopy. Stacks covering the complete distance from the basal to the luminal side (toward the vaginal cavity) were acquired, and the sheets were reconstructed in the z-section by Imaris software.(I) In a typical sheet, nearly all cells were alive, staining green, and only few cells at the luminal side were dead, staining red, which represent naturally dying cells that slough off into the vaginal cavity in vivo (two white arrows).(J) Treatment for 1 hr with 1% sodium azide killed all cells, as demonstrated by loss of the green live cell stain and universal acquisition of the red dead cell marker. |
PMC1885958_fig1_11433.jpg | Describe the main subject of this image. | Separation of Vaginal Epithelial Sheets(A) Photograph of suction blisters on surgically excised vaginal mucosa.(B) Hematoxylin-eosin stain of intact suction blister by light microscopy.(C) Blister roofs, i.e., epithelial sheets, floating in PBS after removal from the underlying stroma, visualized under a stereoscope.(D) Epithelial sheets, separated by EDTA treatment.(E) Stereoscopic view of the basal side of a sheet separated by vacuum suction. An organized pattern of rete ridges and depressions, corresponding to the stromal papillae that were pulled out during separation, can be seen.(F) Stereoscopic view of the basal side of an EDTA-separated sheet, exhibiting the same pattern.(G and H) Toluidine blue-stained cross-section of epithelial sheets separated by vacuum suction (G) or ETDA (H), viewed by light microscopy. In the EDTA sheet, the enucleated outer epithelial cells have swollen during the overnight incubation.(I and J) Live/dead cell staining of EDTA-separated sheets. Sheets were stained with calcein AM (live cells, green), ethidium homodimer-1 (nuclei of dead cells, red), and TOPRO-3 (nuclear counterstain, blue) as described in the manufacturer's protocol. Sheets were immersed in glycerol under a coverslip and imaged by confocal microscopy. Stacks covering the complete distance from the basal to the luminal side (toward the vaginal cavity) were acquired, and the sheets were reconstructed in the z-section by Imaris software.(I) In a typical sheet, nearly all cells were alive, staining green, and only few cells at the luminal side were dead, staining red, which represent naturally dying cells that slough off into the vaginal cavity in vivo (two white arrows).(J) Treatment for 1 hr with 1% sodium azide killed all cells, as demonstrated by loss of the green live cell stain and universal acquisition of the red dead cell marker. |
PMC1885958_fig1_11435.jpg | What's the most prominent thing you notice in this picture? | Separation of Vaginal Epithelial Sheets(A) Photograph of suction blisters on surgically excised vaginal mucosa.(B) Hematoxylin-eosin stain of intact suction blister by light microscopy.(C) Blister roofs, i.e., epithelial sheets, floating in PBS after removal from the underlying stroma, visualized under a stereoscope.(D) Epithelial sheets, separated by EDTA treatment.(E) Stereoscopic view of the basal side of a sheet separated by vacuum suction. An organized pattern of rete ridges and depressions, corresponding to the stromal papillae that were pulled out during separation, can be seen.(F) Stereoscopic view of the basal side of an EDTA-separated sheet, exhibiting the same pattern.(G and H) Toluidine blue-stained cross-section of epithelial sheets separated by vacuum suction (G) or ETDA (H), viewed by light microscopy. In the EDTA sheet, the enucleated outer epithelial cells have swollen during the overnight incubation.(I and J) Live/dead cell staining of EDTA-separated sheets. Sheets were stained with calcein AM (live cells, green), ethidium homodimer-1 (nuclei of dead cells, red), and TOPRO-3 (nuclear counterstain, blue) as described in the manufacturer's protocol. Sheets were immersed in glycerol under a coverslip and imaged by confocal microscopy. Stacks covering the complete distance from the basal to the luminal side (toward the vaginal cavity) were acquired, and the sheets were reconstructed in the z-section by Imaris software.(I) In a typical sheet, nearly all cells were alive, staining green, and only few cells at the luminal side were dead, staining red, which represent naturally dying cells that slough off into the vaginal cavity in vivo (two white arrows).(J) Treatment for 1 hr with 1% sodium azide killed all cells, as demonstrated by loss of the green live cell stain and universal acquisition of the red dead cell marker. |
PMC1885958_fig2_11447.jpg | What is the core subject represented in this visual? | Binding and Entry of HIV-1 in Intraepithelial Vaginal T CellsSuction blister sheets were spinoculated for 2 hr with GFP-Vpr-tagged HIV-1JR-CSF, stained for cell-specific markers and analyzed by confocal microscopy. GFP+ virions are shown in green and CD4 in red. Yellow (or white in [E]) signifies coexpression of GFP and CD4. The blue nuclear counterstain is TOPRO-3.(A–C) Clusters of virion binding CD4+ T cells in the vaginal epithelium in two donors ([A] and [B], donor 1; [C], donor 2).(D) Blocking of viral binding with antibodies to CD4 (αCD4) or CCR5 (αCCR5). Viral binding was quantified with an algorithm given in Supplemental Experimental Procedures online. Each dot depicts the percent GFP+ T cells among all CD4+ T cells counted in a distinct, nonoverlapping confocal stack. Each color signifies stacks acquired in the same tissue donor. Horizontal black bars represent the means calculated from the average percentages in each donor. Mock versus αCD4 and αCCR5 blocking (p = 0.007) was evaluated for significance as described in Experimental Procedures. ΔEnv HIV-1 lacks the viral envelope.(E) Three-dimensional reconstruction from a confocal image stack of an intraepithelial CD4+ T cell by Imaris software. The cell was virtually clipped at its widest circumference so that the green virions located inside the cytoplasm, between the red cell membrane and the blue nucleus, can be clearly identified (yellow arrows). Areas where HIV-1 penetrates the cell membrane, signified by CD4 and HIV-1 colocalization, are shown in white color. The nucleus is rendered as an isosurface and virions appear to enter it at one location (white arrowhead).(F–H) Three representative CD4+ T cells exhibiting cytoplasmic entry of virions. Confocal stacks of individual cells were deconvolved with Autodeblur, and viral entry was determined with an algorithm described in Supplemental Experimental Procedures online. The yellow arrowheads in the magnified insets point to areas of viral entry where GFP+ virions are located on the cytoplasmic side along a section of the cell membrane costaining for CD4 and GFP. |
PMC1885958_fig2_11441.jpg | What does this image primarily show? | Binding and Entry of HIV-1 in Intraepithelial Vaginal T CellsSuction blister sheets were spinoculated for 2 hr with GFP-Vpr-tagged HIV-1JR-CSF, stained for cell-specific markers and analyzed by confocal microscopy. GFP+ virions are shown in green and CD4 in red. Yellow (or white in [E]) signifies coexpression of GFP and CD4. The blue nuclear counterstain is TOPRO-3.(A–C) Clusters of virion binding CD4+ T cells in the vaginal epithelium in two donors ([A] and [B], donor 1; [C], donor 2).(D) Blocking of viral binding with antibodies to CD4 (αCD4) or CCR5 (αCCR5). Viral binding was quantified with an algorithm given in Supplemental Experimental Procedures online. Each dot depicts the percent GFP+ T cells among all CD4+ T cells counted in a distinct, nonoverlapping confocal stack. Each color signifies stacks acquired in the same tissue donor. Horizontal black bars represent the means calculated from the average percentages in each donor. Mock versus αCD4 and αCCR5 blocking (p = 0.007) was evaluated for significance as described in Experimental Procedures. ΔEnv HIV-1 lacks the viral envelope.(E) Three-dimensional reconstruction from a confocal image stack of an intraepithelial CD4+ T cell by Imaris software. The cell was virtually clipped at its widest circumference so that the green virions located inside the cytoplasm, between the red cell membrane and the blue nucleus, can be clearly identified (yellow arrows). Areas where HIV-1 penetrates the cell membrane, signified by CD4 and HIV-1 colocalization, are shown in white color. The nucleus is rendered as an isosurface and virions appear to enter it at one location (white arrowhead).(F–H) Three representative CD4+ T cells exhibiting cytoplasmic entry of virions. Confocal stacks of individual cells were deconvolved with Autodeblur, and viral entry was determined with an algorithm described in Supplemental Experimental Procedures online. The yellow arrowheads in the magnified insets point to areas of viral entry where GFP+ virions are located on the cytoplasmic side along a section of the cell membrane costaining for CD4 and GFP. |
PMC1885958_fig2_11443.jpg | What is the core subject represented in this visual? | Binding and Entry of HIV-1 in Intraepithelial Vaginal T CellsSuction blister sheets were spinoculated for 2 hr with GFP-Vpr-tagged HIV-1JR-CSF, stained for cell-specific markers and analyzed by confocal microscopy. GFP+ virions are shown in green and CD4 in red. Yellow (or white in [E]) signifies coexpression of GFP and CD4. The blue nuclear counterstain is TOPRO-3.(A–C) Clusters of virion binding CD4+ T cells in the vaginal epithelium in two donors ([A] and [B], donor 1; [C], donor 2).(D) Blocking of viral binding with antibodies to CD4 (αCD4) or CCR5 (αCCR5). Viral binding was quantified with an algorithm given in Supplemental Experimental Procedures online. Each dot depicts the percent GFP+ T cells among all CD4+ T cells counted in a distinct, nonoverlapping confocal stack. Each color signifies stacks acquired in the same tissue donor. Horizontal black bars represent the means calculated from the average percentages in each donor. Mock versus αCD4 and αCCR5 blocking (p = 0.007) was evaluated for significance as described in Experimental Procedures. ΔEnv HIV-1 lacks the viral envelope.(E) Three-dimensional reconstruction from a confocal image stack of an intraepithelial CD4+ T cell by Imaris software. The cell was virtually clipped at its widest circumference so that the green virions located inside the cytoplasm, between the red cell membrane and the blue nucleus, can be clearly identified (yellow arrows). Areas where HIV-1 penetrates the cell membrane, signified by CD4 and HIV-1 colocalization, are shown in white color. The nucleus is rendered as an isosurface and virions appear to enter it at one location (white arrowhead).(F–H) Three representative CD4+ T cells exhibiting cytoplasmic entry of virions. Confocal stacks of individual cells were deconvolved with Autodeblur, and viral entry was determined with an algorithm described in Supplemental Experimental Procedures online. The yellow arrowheads in the magnified insets point to areas of viral entry where GFP+ virions are located on the cytoplasmic side along a section of the cell membrane costaining for CD4 and GFP. |
PMC1885958_fig2_11446.jpg | What is the principal component of this image? | Binding and Entry of HIV-1 in Intraepithelial Vaginal T CellsSuction blister sheets were spinoculated for 2 hr with GFP-Vpr-tagged HIV-1JR-CSF, stained for cell-specific markers and analyzed by confocal microscopy. GFP+ virions are shown in green and CD4 in red. Yellow (or white in [E]) signifies coexpression of GFP and CD4. The blue nuclear counterstain is TOPRO-3.(A–C) Clusters of virion binding CD4+ T cells in the vaginal epithelium in two donors ([A] and [B], donor 1; [C], donor 2).(D) Blocking of viral binding with antibodies to CD4 (αCD4) or CCR5 (αCCR5). Viral binding was quantified with an algorithm given in Supplemental Experimental Procedures online. Each dot depicts the percent GFP+ T cells among all CD4+ T cells counted in a distinct, nonoverlapping confocal stack. Each color signifies stacks acquired in the same tissue donor. Horizontal black bars represent the means calculated from the average percentages in each donor. Mock versus αCD4 and αCCR5 blocking (p = 0.007) was evaluated for significance as described in Experimental Procedures. ΔEnv HIV-1 lacks the viral envelope.(E) Three-dimensional reconstruction from a confocal image stack of an intraepithelial CD4+ T cell by Imaris software. The cell was virtually clipped at its widest circumference so that the green virions located inside the cytoplasm, between the red cell membrane and the blue nucleus, can be clearly identified (yellow arrows). Areas where HIV-1 penetrates the cell membrane, signified by CD4 and HIV-1 colocalization, are shown in white color. The nucleus is rendered as an isosurface and virions appear to enter it at one location (white arrowhead).(F–H) Three representative CD4+ T cells exhibiting cytoplasmic entry of virions. Confocal stacks of individual cells were deconvolved with Autodeblur, and viral entry was determined with an algorithm described in Supplemental Experimental Procedures online. The yellow arrowheads in the magnified insets point to areas of viral entry where GFP+ virions are located on the cytoplasmic side along a section of the cell membrane costaining for CD4 and GFP. |
PMC1885958_fig2_11444.jpg | What is being portrayed in this visual content? | Binding and Entry of HIV-1 in Intraepithelial Vaginal T CellsSuction blister sheets were spinoculated for 2 hr with GFP-Vpr-tagged HIV-1JR-CSF, stained for cell-specific markers and analyzed by confocal microscopy. GFP+ virions are shown in green and CD4 in red. Yellow (or white in [E]) signifies coexpression of GFP and CD4. The blue nuclear counterstain is TOPRO-3.(A–C) Clusters of virion binding CD4+ T cells in the vaginal epithelium in two donors ([A] and [B], donor 1; [C], donor 2).(D) Blocking of viral binding with antibodies to CD4 (αCD4) or CCR5 (αCCR5). Viral binding was quantified with an algorithm given in Supplemental Experimental Procedures online. Each dot depicts the percent GFP+ T cells among all CD4+ T cells counted in a distinct, nonoverlapping confocal stack. Each color signifies stacks acquired in the same tissue donor. Horizontal black bars represent the means calculated from the average percentages in each donor. Mock versus αCD4 and αCCR5 blocking (p = 0.007) was evaluated for significance as described in Experimental Procedures. ΔEnv HIV-1 lacks the viral envelope.(E) Three-dimensional reconstruction from a confocal image stack of an intraepithelial CD4+ T cell by Imaris software. The cell was virtually clipped at its widest circumference so that the green virions located inside the cytoplasm, between the red cell membrane and the blue nucleus, can be clearly identified (yellow arrows). Areas where HIV-1 penetrates the cell membrane, signified by CD4 and HIV-1 colocalization, are shown in white color. The nucleus is rendered as an isosurface and virions appear to enter it at one location (white arrowhead).(F–H) Three representative CD4+ T cells exhibiting cytoplasmic entry of virions. Confocal stacks of individual cells were deconvolved with Autodeblur, and viral entry was determined with an algorithm described in Supplemental Experimental Procedures online. The yellow arrowheads in the magnified insets point to areas of viral entry where GFP+ virions are located on the cytoplasmic side along a section of the cell membrane costaining for CD4 and GFP. |
PMC1887524_F2_11475.jpg | What is the focal point of this photograph? | * Muscle involvement in the lower limbs in CCD secondary to dominant RYR1 mutations: T1-weighted MR imaging, transverse sections of the proximal thigh (A-C) and the proximal lower leg (D-F) in an eleven (A) and a thirteen year old boy (B,E), and a twelve (C,F) and seventeen year old girl (D). In the thigh (A-C), there is marked increase in abnormal signal within vasti, sartorius and adductor magnus with relative sparing of rectus femoris, adductor longus, gracilis and semitendinosus. In the lower leg, there is increase in abnormal signal in soleus (D-F), and – in more severe cases (E-F) – peroneal group and gastrocnemius medialis. Tibialis anterior and gastrocnemius lateralis are relatively spared. (VL = vastus lateralis, VI = vastus intermedius, VM = vastus medialis, RF = rectus femoris, AL = adductor longus, AM = adductor magnus, S = sartorius, G = gracilis, St = semitendinosus). * Reprinted from Neuromuscul Disord 2004, 14: Jungbluth H, Davis MR, Muller C, Counsell S, Allsop J, Chattopadhyay A, Messina S, Mercuri E, Laing NG, Sewry CA, Bydder G, Muntoni F. Magnetic resonance imaging of muscle in congenital myopathies associated with RYR1 mutations. Pages: 785–790. Copyright Owner Elsevier, Copyright (2004), with permission from Elsevier". |
PMC1887524_F2_11471.jpg | What stands out most in this visual? | * Muscle involvement in the lower limbs in CCD secondary to dominant RYR1 mutations: T1-weighted MR imaging, transverse sections of the proximal thigh (A-C) and the proximal lower leg (D-F) in an eleven (A) and a thirteen year old boy (B,E), and a twelve (C,F) and seventeen year old girl (D). In the thigh (A-C), there is marked increase in abnormal signal within vasti, sartorius and adductor magnus with relative sparing of rectus femoris, adductor longus, gracilis and semitendinosus. In the lower leg, there is increase in abnormal signal in soleus (D-F), and – in more severe cases (E-F) – peroneal group and gastrocnemius medialis. Tibialis anterior and gastrocnemius lateralis are relatively spared. (VL = vastus lateralis, VI = vastus intermedius, VM = vastus medialis, RF = rectus femoris, AL = adductor longus, AM = adductor magnus, S = sartorius, G = gracilis, St = semitendinosus). * Reprinted from Neuromuscul Disord 2004, 14: Jungbluth H, Davis MR, Muller C, Counsell S, Allsop J, Chattopadhyay A, Messina S, Mercuri E, Laing NG, Sewry CA, Bydder G, Muntoni F. Magnetic resonance imaging of muscle in congenital myopathies associated with RYR1 mutations. Pages: 785–790. Copyright Owner Elsevier, Copyright (2004), with permission from Elsevier". |
PMC1887524_F2_11474.jpg | What does this image primarily show? | * Muscle involvement in the lower limbs in CCD secondary to dominant RYR1 mutations: T1-weighted MR imaging, transverse sections of the proximal thigh (A-C) and the proximal lower leg (D-F) in an eleven (A) and a thirteen year old boy (B,E), and a twelve (C,F) and seventeen year old girl (D). In the thigh (A-C), there is marked increase in abnormal signal within vasti, sartorius and adductor magnus with relative sparing of rectus femoris, adductor longus, gracilis and semitendinosus. In the lower leg, there is increase in abnormal signal in soleus (D-F), and – in more severe cases (E-F) – peroneal group and gastrocnemius medialis. Tibialis anterior and gastrocnemius lateralis are relatively spared. (VL = vastus lateralis, VI = vastus intermedius, VM = vastus medialis, RF = rectus femoris, AL = adductor longus, AM = adductor magnus, S = sartorius, G = gracilis, St = semitendinosus). * Reprinted from Neuromuscul Disord 2004, 14: Jungbluth H, Davis MR, Muller C, Counsell S, Allsop J, Chattopadhyay A, Messina S, Mercuri E, Laing NG, Sewry CA, Bydder G, Muntoni F. Magnetic resonance imaging of muscle in congenital myopathies associated with RYR1 mutations. Pages: 785–790. Copyright Owner Elsevier, Copyright (2004), with permission from Elsevier". |
PMC1887524_F2_11472.jpg | What is the core subject represented in this visual? | * Muscle involvement in the lower limbs in CCD secondary to dominant RYR1 mutations: T1-weighted MR imaging, transverse sections of the proximal thigh (A-C) and the proximal lower leg (D-F) in an eleven (A) and a thirteen year old boy (B,E), and a twelve (C,F) and seventeen year old girl (D). In the thigh (A-C), there is marked increase in abnormal signal within vasti, sartorius and adductor magnus with relative sparing of rectus femoris, adductor longus, gracilis and semitendinosus. In the lower leg, there is increase in abnormal signal in soleus (D-F), and – in more severe cases (E-F) – peroneal group and gastrocnemius medialis. Tibialis anterior and gastrocnemius lateralis are relatively spared. (VL = vastus lateralis, VI = vastus intermedius, VM = vastus medialis, RF = rectus femoris, AL = adductor longus, AM = adductor magnus, S = sartorius, G = gracilis, St = semitendinosus). * Reprinted from Neuromuscul Disord 2004, 14: Jungbluth H, Davis MR, Muller C, Counsell S, Allsop J, Chattopadhyay A, Messina S, Mercuri E, Laing NG, Sewry CA, Bydder G, Muntoni F. Magnetic resonance imaging of muscle in congenital myopathies associated with RYR1 mutations. Pages: 785–790. Copyright Owner Elsevier, Copyright (2004), with permission from Elsevier". |
PMC1887527_F2_11468.jpg | What's the most prominent thing you notice in this picture? | Contrast enhanced MRI of the right knee demonstrating chronic inflammation with synovial thickening. |
PMC1887527_F3_11470.jpg | What object or scene is depicted here? | Contrast enhanced MRI of the left knee demonstrating chronic inflammation with synovial thickening. |
PMC1887528_F4_11477.jpg | What is shown in this image? | Osgood-Schlatter disease. Lateral radiograph of the knee demonstrating fragmentation of the tibial tubercle with overlying soft tissue swelling. (Radiograph courtesy of BC Children's Hospital) |
PMC1888687_F5_11478.jpg | What is the main focus of this visual representation? | Treatment with ML-7 causes cleavage furrow regression. (A) Time-course of a dividing Drosophila spermatocyte treated with 80 μM ML-7 just after the time-point depicted in the second panel. The cell was washed with Insect Ringer's buffer just after the time-point depicted in the fourth panel. Bar, 10 μm. (B) Plot of the change in cell diameter (ordinate) over time (abscissa) for the Drosophila spermatocyte shown in A. Time-points of ML-7 addition (left arrow) and washout (right arrow) are indicated [see Additional file 9]. |
PMC1888687_F5_11483.jpg | What is the main focus of this visual representation? | Treatment with ML-7 causes cleavage furrow regression. (A) Time-course of a dividing Drosophila spermatocyte treated with 80 μM ML-7 just after the time-point depicted in the second panel. The cell was washed with Insect Ringer's buffer just after the time-point depicted in the fourth panel. Bar, 10 μm. (B) Plot of the change in cell diameter (ordinate) over time (abscissa) for the Drosophila spermatocyte shown in A. Time-points of ML-7 addition (left arrow) and washout (right arrow) are indicated [see Additional file 9]. |
PMC1888687_F5_11479.jpg | Can you identify the primary element in this image? | Treatment with ML-7 causes cleavage furrow regression. (A) Time-course of a dividing Drosophila spermatocyte treated with 80 μM ML-7 just after the time-point depicted in the second panel. The cell was washed with Insect Ringer's buffer just after the time-point depicted in the fourth panel. Bar, 10 μm. (B) Plot of the change in cell diameter (ordinate) over time (abscissa) for the Drosophila spermatocyte shown in A. Time-points of ML-7 addition (left arrow) and washout (right arrow) are indicated [see Additional file 9]. |
PMC1888726_pone-0000536-g003_11484.jpg | What is the central feature of this picture? | Immunohistochemical identification of phospho-tau positive dystrophic neurites in Tg2576:sod2 mice.(a) Immunohistochemistry for anti Ser-396 was carried out as described in the text, and positivity was observed surrounding senile plaques in the brains of Tg2576:sod2 mice. (b) In order to ensure specificity, we also tested the effects of preadsorbing the Ser-396 antibody with the peptide the antibody was raised against. This abolished the staining seen around the plaques. |
PMC1890004_fig3_11493.jpg | What is shown in this image? | Functional Localization of JR's LesionFunctional images for oculomotor activity (upper panels) or manual activity (lower panels) were acquired at 1.5T (left panels) and at 7T (right panels). For 1.5T, statistical contrasts (thresholded at p < 0.001 uncorrected) are superimposed on a T2-weighted sagittal image acquired with resolution 1.6 × 0.575 × 0.575 mm. The high-resolution 7T functional maps (1 × 1 × 3 mm) are superimposed on the mean echoplanar image. The scale bars indicate the very small size of the lesion (note also that there is likely to have been signal dropout around the true lesion due to hemosiderin deposition). There is clear contralesional oculomotor activity precisely opposite the lesion, indicating that the ipsilesional SEF is damaged. The extent of damage to the SMA is less clear but is likely to be less than to the SEF, given the rostral position and small size of the lesion. See text for more details. See Supplemental Data for clinical information and imaging methodology. |
PMC1890004_fig3_11495.jpg | What is being portrayed in this visual content? | Functional Localization of JR's LesionFunctional images for oculomotor activity (upper panels) or manual activity (lower panels) were acquired at 1.5T (left panels) and at 7T (right panels). For 1.5T, statistical contrasts (thresholded at p < 0.001 uncorrected) are superimposed on a T2-weighted sagittal image acquired with resolution 1.6 × 0.575 × 0.575 mm. The high-resolution 7T functional maps (1 × 1 × 3 mm) are superimposed on the mean echoplanar image. The scale bars indicate the very small size of the lesion (note also that there is likely to have been signal dropout around the true lesion due to hemosiderin deposition). There is clear contralesional oculomotor activity precisely opposite the lesion, indicating that the ipsilesional SEF is damaged. The extent of damage to the SMA is less clear but is likely to be less than to the SEF, given the rostral position and small size of the lesion. See text for more details. See Supplemental Data for clinical information and imaging methodology. |
PMC1890004_fig3_11492.jpg | What is the dominant medical problem in this image? | Functional Localization of JR's LesionFunctional images for oculomotor activity (upper panels) or manual activity (lower panels) were acquired at 1.5T (left panels) and at 7T (right panels). For 1.5T, statistical contrasts (thresholded at p < 0.001 uncorrected) are superimposed on a T2-weighted sagittal image acquired with resolution 1.6 × 0.575 × 0.575 mm. The high-resolution 7T functional maps (1 × 1 × 3 mm) are superimposed on the mean echoplanar image. The scale bars indicate the very small size of the lesion (note also that there is likely to have been signal dropout around the true lesion due to hemosiderin deposition). There is clear contralesional oculomotor activity precisely opposite the lesion, indicating that the ipsilesional SEF is damaged. The extent of damage to the SMA is less clear but is likely to be less than to the SEF, given the rostral position and small size of the lesion. See text for more details. See Supplemental Data for clinical information and imaging methodology. |
PMC1890004_fig3_11496.jpg | What stands out most in this visual? | Functional Localization of JR's LesionFunctional images for oculomotor activity (upper panels) or manual activity (lower panels) were acquired at 1.5T (left panels) and at 7T (right panels). For 1.5T, statistical contrasts (thresholded at p < 0.001 uncorrected) are superimposed on a T2-weighted sagittal image acquired with resolution 1.6 × 0.575 × 0.575 mm. The high-resolution 7T functional maps (1 × 1 × 3 mm) are superimposed on the mean echoplanar image. The scale bars indicate the very small size of the lesion (note also that there is likely to have been signal dropout around the true lesion due to hemosiderin deposition). There is clear contralesional oculomotor activity precisely opposite the lesion, indicating that the ipsilesional SEF is damaged. The extent of damage to the SMA is less clear but is likely to be less than to the SEF, given the rostral position and small size of the lesion. See text for more details. See Supplemental Data for clinical information and imaging methodology. |
PMC1890004_fig3_11499.jpg | What's the most prominent thing you notice in this picture? | Functional Localization of JR's LesionFunctional images for oculomotor activity (upper panels) or manual activity (lower panels) were acquired at 1.5T (left panels) and at 7T (right panels). For 1.5T, statistical contrasts (thresholded at p < 0.001 uncorrected) are superimposed on a T2-weighted sagittal image acquired with resolution 1.6 × 0.575 × 0.575 mm. The high-resolution 7T functional maps (1 × 1 × 3 mm) are superimposed on the mean echoplanar image. The scale bars indicate the very small size of the lesion (note also that there is likely to have been signal dropout around the true lesion due to hemosiderin deposition). There is clear contralesional oculomotor activity precisely opposite the lesion, indicating that the ipsilesional SEF is damaged. The extent of damage to the SMA is less clear but is likely to be less than to the SEF, given the rostral position and small size of the lesion. See text for more details. See Supplemental Data for clinical information and imaging methodology. |
PMC1890004_fig4_11489.jpg | What's the most prominent thing you notice in this picture? | Control Patients' LesionsFunctional imaging for oculomotor activity in patient AG (left panel) demonstrates SEF activation in the lesioned hemisphere caudal to the lesion. Thus pre-SMA is damaged, but not SEF and SMA. Sagittal structural images to either side of midline (right panels) reveal the extent of surgical resection in AG. Patient VC and patient RS have extensive strokes involving lateral frontal cortex, including ventral and dorsal premotor regions, but no involvement of medial frontal cortex. See Supplemental Data for clinical information and imaging methodology. |
PMC1890004_fig4_11490.jpg | Describe the main subject of this image. | Control Patients' LesionsFunctional imaging for oculomotor activity in patient AG (left panel) demonstrates SEF activation in the lesioned hemisphere caudal to the lesion. Thus pre-SMA is damaged, but not SEF and SMA. Sagittal structural images to either side of midline (right panels) reveal the extent of surgical resection in AG. Patient VC and patient RS have extensive strokes involving lateral frontal cortex, including ventral and dorsal premotor regions, but no involvement of medial frontal cortex. See Supplemental Data for clinical information and imaging methodology. |
PMC1890004_fig4_11488.jpg | What can you see in this picture? | Control Patients' LesionsFunctional imaging for oculomotor activity in patient AG (left panel) demonstrates SEF activation in the lesioned hemisphere caudal to the lesion. Thus pre-SMA is damaged, but not SEF and SMA. Sagittal structural images to either side of midline (right panels) reveal the extent of surgical resection in AG. Patient VC and patient RS have extensive strokes involving lateral frontal cortex, including ventral and dorsal premotor regions, but no involvement of medial frontal cortex. See Supplemental Data for clinical information and imaging methodology. |
PMC1890292_F7_11505.jpg | What is shown in this image? | Regeneration of melanophores after skin grafting in tadpoles. (A) A piece of GFP-labelled skin was grafted to the lateral region of the middle trunk of a non-GFP tadpole host, which was then amputated 3 days after. (B) A 7 day tail regenerate from a skin grafted tadpole, white arrowheads indicate the amputation level. (C) Detection of GFP in a melanophore in the regenerate. 4 views are shown: top left transmitted light; top right GFP fluorescence; bottom left DAPI fluorescence (DNA); bottom right transmitted light and fluorescence. Scale bars: 500 μm in A, B, 10 μm in C. |
PMC1890292_F7_11504.jpg | What key item or scene is captured in this photo? | Regeneration of melanophores after skin grafting in tadpoles. (A) A piece of GFP-labelled skin was grafted to the lateral region of the middle trunk of a non-GFP tadpole host, which was then amputated 3 days after. (B) A 7 day tail regenerate from a skin grafted tadpole, white arrowheads indicate the amputation level. (C) Detection of GFP in a melanophore in the regenerate. 4 views are shown: top left transmitted light; top right GFP fluorescence; bottom left DAPI fluorescence (DNA); bottom right transmitted light and fluorescence. Scale bars: 500 μm in A, B, 10 μm in C. |
PMC1890292_F7_11502.jpg | What is the principal component of this image? | Regeneration of melanophores after skin grafting in tadpoles. (A) A piece of GFP-labelled skin was grafted to the lateral region of the middle trunk of a non-GFP tadpole host, which was then amputated 3 days after. (B) A 7 day tail regenerate from a skin grafted tadpole, white arrowheads indicate the amputation level. (C) Detection of GFP in a melanophore in the regenerate. 4 views are shown: top left transmitted light; top right GFP fluorescence; bottom left DAPI fluorescence (DNA); bottom right transmitted light and fluorescence. Scale bars: 500 μm in A, B, 10 μm in C. |
PMC1890305_pone-0000546-g002_11506.jpg | What is the central feature of this picture? | Neural Interaction of Emotion and Feedback Veracity.Left; Significant interactions of emotion (happy neutral) and feedback (true false) were observed on neural activity within; 1) right anterior insula, 2) right amygdala, 3)left amygdala, 4)right mid insula, 5) left mid insula and 6) posterior dorsal cerebellum. Functional interactions are projected onto a normalised mean structural image calculated from each individual subjects structural T1 weighted image. Dashed bounding box illustrates volume of acquired T2 data. Right; Contrast estimates at the illustrated regions are displayed. |
PMC1890305_pone-0000546-g002_11509.jpg | What is shown in this image? | Neural Interaction of Emotion and Feedback Veracity.Left; Significant interactions of emotion (happy neutral) and feedback (true false) were observed on neural activity within; 1) right anterior insula, 2) right amygdala, 3)left amygdala, 4)right mid insula, 5) left mid insula and 6) posterior dorsal cerebellum. Functional interactions are projected onto a normalised mean structural image calculated from each individual subjects structural T1 weighted image. Dashed bounding box illustrates volume of acquired T2 data. Right; Contrast estimates at the illustrated regions are displayed. |
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