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So the genetic code basically is the link between the sequence of nucleotides and our sequence of amino acids. | The Genetic Code.txt |
Now, what exactly does our genetic code actually consist of? | The Genetic Code.txt |
Well, basically, the genetic code is a list of codons. | The Genetic Code.txt |
And a codon is basically a series of three consecutive nucleotides, where each codon corresponds to specific type of amino acids. | The Genetic Code.txt |
So in the mRNA molecule, a series of three consecutive nucleotides, known as our codon, corresponds to some specific amino acid. | The Genetic Code.txt |
For example, the sequence of nucleotides, our guanine, uracil. | The Genetic Code.txt |
Uracil, corresponds to a specific amino acid known as valine. | The Genetic Code.txt |
So to see what we mean, let's take a look at the following diagram. | The Genetic Code.txt |
So, let's suppose our ribosomes in the cell take the following mRNA. | The Genetic Code.txt |
And what the ribosomes do is they use our genetic code to basically translate what these codons correspond to. | The Genetic Code.txt |
So the codon guu, the sequence of Guamine uracil uracil, always corresponds to the amino acid valine, while the sequence CCU always corresponds to our amino acid proline. | The Genetic Code.txt |
So we see that our genetic code links our mRNA molecule to our protein, and that's exactly how we synthesize or translate our proteins. | The Genetic Code.txt |
Now, the question you might be wondering is, why is our codon exactly three nucleotides? | The Genetic Code.txt |
Why isn't the sequence only two nucleotides? | The Genetic Code.txt |
Well, to answer this question, we can use simple mathematics. | The Genetic Code.txt |
We can use simple combinatorics. | The Genetic Code.txt |
So recall that proteins consist of 20 different amino acids. | The Genetic Code.txt |
So we have 20 different amino acids that our body, as well as other organisms actually use. | The Genetic Code.txt |
So that means if the genetic code actually makes sense, then we better have 20 different unique codons that correspond to 20 different unique amino acids that appear in our body. | The Genetic Code.txt |
But if we use simple math, we see that if we only have two different positions, two different nucleotides in our codon, then the maximum number of different types of codons is 16. | The Genetic Code.txt |
And that's because we have four different possibilities for nucleotides. | The Genetic Code.txt |
And four times four gives us 16. | The Genetic Code.txt |
And 16 is not enough to actually correspond to the 20 different amino acids that exist in nature. | The Genetic Code.txt |
And that's exactly why we have to add one more nucleotide so that we have three consecutive nucleotides in our codon sequence, because four times four times four gives us 64 possibilities. | The Genetic Code.txt |
And that is enough to basically describe the 20 different amino acids that exist in nature. | The Genetic Code.txt |
Now, right away, you should notice that the genetic code contains 64 different codons in that particular genetic code. | The Genetic Code.txt |
So 64 different variations of three letter sequences of nucleotides. | The Genetic Code.txt |
And since there are only 20 different amino acids that exist in nature, that implies that many of the three letter codons correspond to the same exact amino acid. | The Genetic Code.txt |
And this phenomenon, the fact that two or more different codons can correspond to the same exact amino acid, makes our genetic code redundant or degenerate. | The Genetic Code.txt |
So, basically, if we look at the following diagram, it describes what we just mentioned. | The Genetic Code.txt |
So if we take our genetic code, we see that the sequence CC, you or cytosine cytosine yourself, and the sequence Cytosine cytosine cytosine or CCC, these two different sequences, both correspond to the same exact amino acid. | The Genetic Code.txt |
They correspond to our amino acid proline. | The Genetic Code.txt |
Now, I haven't actually listed all the codons that are found in the genetic code, but if you want to, you can look up our genetic code online or in a textbook. | The Genetic Code.txt |
So, once again, as we'll see in the next several lectures, during the process of translation, when we synthesize our proteins from mRNA molecules, we have to have a way to translate the language used by the mRNA to the language that is used by the proteins. | The Genetic Code.txt |
And what the ribosomes do is they use this system known as the genetic code, in which we basically have three letter sequences that are known as codons that correspond to specific amino acids. | The Genetic Code.txt |
And the genetic code is set to be redundant or degenerate, which basically means that two or more different codons can correspond to the same exact amino acid. | The Genetic Code.txt |
And this makes sense because we only have 20 amino acids and we have 64 different combinations for our codons. | The Genetic Code.txt |
Our wing type gene. | Gene Mapping, Recombination and Map Units Part II.txt |
And we have this gene right here. | Gene Mapping, Recombination and Map Units Part II.txt |
That is our color gene. | Gene Mapping, Recombination and Map Units Part II.txt |
So we have the color gene and we have the wing type gene. | Gene Mapping, Recombination and Map Units Part II.txt |
Okay, this distance here, given in Map units is equal to ten Map units or ten recombination units. | Gene Mapping, Recombination and Map Units Part II.txt |
Now, it's important to remember that Map units do not actually give us a physical distance, but the Map units are correlated. | Gene Mapping, Recombination and Map Units Part II.txt |
They're related to the physical distance. | Gene Mapping, Recombination and Map Units Part II.txt |
And what that means is, the greater the number of Map units, the greater the number of recombination units, the greater the distances between those two particular genes on that given in chromosome. | Gene Mapping, Recombination and Map Units Part II.txt |
The cells of our body depend on signal transduction pathways to carry out different types of cell processes at the right moments in time to basically produce physiological responses to certain types of external stimuli. | Cancer and Termination of Signal Pathways .txt |
Now, even though these signal transduction pathways are very, very important to the functionality of our cells, these signal transduction pathways must, must be closely maintained and regulated by ourselves. | Cancer and Termination of Signal Pathways .txt |
In fact, the inability of our cells to regulate and terminate these signal transduction pathways can actually lead to tumor growth and eventually cancer. | Cancer and Termination of Signal Pathways .txt |
And so in this lecture, what I'd like to focus on is discuss how different types of abnormalities in a signal transduction pathway can actually lead to cancer. | Cancer and Termination of Signal Pathways .txt |
Now, before we actually begin our discussion on the abnormality part, let's focus on how normal process takes place and how normally our cells terminate these signal transduction pathways. | Cancer and Termination of Signal Pathways .txt |
And to use an example, we're going to focus on the EGF signal transduction pathway where EGF stands for Epidermal growth factor. | Cancer and Termination of Signal Pathways .txt |
Remember, this is the pathway used by the cells that ultimately stimulates the growth and division of epithelial and epidermal cells. | Cancer and Termination of Signal Pathways .txt |
So let's begin by focusing on how this pathway actually takes place, beginning with the binding of the EGF molecules onto their domains. | Cancer and Termination of Signal Pathways .txt |
So we have two EGF molecules bind onto each one of these domains shown in purple. | Cancer and Termination of Signal Pathways .txt |
And once the binding takes place, these two monomers associate with one another to form a dimer and that creates conformational changes in these two structures found in a cytoplasm. | Cancer and Termination of Signal Pathways .txt |
Now these two structures, and by the way, this is the EGF receptor these two structures actually contain tyrosine protein kinase domains. | Cancer and Termination of Signal Pathways .txt |
And once a conformational change takes place upon binding and the dimerization process, a cross phosphorylation takes place and the carboxyl terminal ends of this tail and this tail are phosphorylated by the active sides of these corresponding kinases. | Cancer and Termination of Signal Pathways .txt |
And once we form these phosphorylated residues, we have an important adaptor protein known as GRB Two that binds onto this section and that calls upon another protein known as SOS. | Cancer and Termination of Signal Pathways .txt |
And what SOS does is it binds an inactive small G protein known as Ras. | Cancer and Termination of Signal Pathways .txt |
When Ras binds unto this structure, there's a conformational change that takes place in the Ras protein and the GDP Guanosine diphosphate is expelled and the GTP Guanosine triphosphate moves into that pocket. | Cancer and Termination of Signal Pathways .txt |
And once GTP binds, that activates that G protein we call Ras. | Cancer and Termination of Signal Pathways .txt |
And once Ras is activated, it moves on and activates a protein kinase we call Raff. | Cancer and Termination of Signal Pathways .txt |
And once this protein kinase is activated, it goes on to form these to activate other protein kinases we call mex the Max. | Cancer and Termination of Signal Pathways .txt |
Once activated, it goes on to activate other protein kinases we call Hercs. | Cancer and Termination of Signal Pathways .txt |
Now these Hercs can actually move into the nucleus of our cell. | Cancer and Termination of Signal Pathways .txt |
So we have this double phospholipid bilayer of the nucleus. | Cancer and Termination of Signal Pathways .txt |
These IRCS go into the cell nucleus and they activate transcription factors. | Cancer and Termination of Signal Pathways .txt |
These transcription factors then move on and express different types of genes that produce mRNA molecules which then exit the cell and they essentially are used by the ribosomes to produce proteins. | Cancer and Termination of Signal Pathways .txt |
The proteins are in turn used to basically build up the cytoplasm, build up the cytoskeleton which basically increases the size of the cell and that cell eventually is able to divide. | Cancer and Termination of Signal Pathways .txt |
And so in this process, the EGF signal transduction pathway stimulates cell differentiation, cell growth and cell proliferation of two types of cells, epidermal cells and epithelial cells. | Cancer and Termination of Signal Pathways .txt |
Now, once this pathway actually carries out its specific purpose, how exactly does a normal cell terminate this process? | Cancer and Termination of Signal Pathways .txt |
Well, there are three major methods. | Cancer and Termination of Signal Pathways .txt |
Method number one is the fact that because we have a G protein involved and G proteins have Gtpa's activity, what that means is they have a built in clock that allows it to actually shut itself down following activation. | Cancer and Termination of Signal Pathways .txt |
So sometime after this has been activated into the GTP form, this green structure, the G protein, because it has Gtph activity, it is able to actually take a water molecule from the cytoplasm and hydrolyze the GTP back into GDP. | Cancer and Termination of Signal Pathways .txt |
And once it inactivates itself, this can no longer stimulate the rest of the process. | Cancer and Termination of Signal Pathways .txt |
And so this pathway essentially shuts down as a result. | Cancer and Termination of Signal Pathways .txt |
So cells can terminate the pathway by using Gtpa's activity of G proteins and that is built in into that molecule. | Cancer and Termination of Signal Pathways .txt |
Number two, these cells can also actually terminate the pathway by using a class of molecules we call phosphatases. | Cancer and Termination of Signal Pathways .txt |
So in fact, as soon as this pathway is activated, it also activates many different types of phosphatases. | Cancer and Termination of Signal Pathways .txt |
And what phosphatases do is they essentially remove us four groups that were attached by protein kinases. | Cancer and Termination of Signal Pathways .txt |
So for instance, we have the Rat, the Mechs, the Irks, and these two structures that act as protein kinases in this particular case. | Cancer and Termination of Signal Pathways .txt |
And what the phosphatases do is they essentially move onto the target proteins and they remove those phosphoryl groups that were placed by all these different protein kinases. | Cancer and Termination of Signal Pathways .txt |
For instance, these phosphatases can remove these phosphoryl groups here and that essentially inactivates this part of the pathway and so it cannot continue and as a result it is shut down. | Cancer and Termination of Signal Pathways .txt |
And so anywhere I have an asterisk, that basically means we're dealing with a protein kinase. | Cancer and Termination of Signal Pathways .txt |
And so these phosphatases can influence and shut down this protein, these proteins, these proteins and also these two structures here which are actually part of that EGF receptor. | Cancer and Termination of Signal Pathways .txt |
And finally we can terminate the pathway by inactivating that receptor of the pathway. | Cancer and Termination of Signal Pathways .txt |
And actually we already spoke about one way by which we can inactivate is by removing these phosphoryl groups. | Cancer and Termination of Signal Pathways .txt |
Another way is if these two ligands actually dissociate. | Cancer and Termination of Signal Pathways .txt |
When the two ligands dissociate, the entire diameter basically breaks apart into monomers and in that particular case it is not as active as in this particular case. | Cancer and Termination of Signal Pathways .txt |
And so what that means is that will decrease the activity of this signal transduction pathway. | Cancer and Termination of Signal Pathways .txt |
So this is the normal way by which the pathway actually is terminated. | Cancer and Termination of Signal Pathways .txt |
But what happens in the abnormal case? | Cancer and Termination of Signal Pathways .txt |
How can an abnormality in each one of these cases, one, two, three, actually lead to the production of tumors and eventually cancer? | Cancer and Termination of Signal Pathways .txt |
So let's focus on number one. | Cancer and Termination of Signal Pathways .txt |
So we said our cells can terminate by using these Gtpas activity G proteins. | Cancer and Termination of Signal Pathways .txt |
So this Rasp protein has a certain gene in the DNA that expresses it. | Cancer and Termination of Signal Pathways .txt |
Now let's suppose the gene is a normal gene and that means this will be a normal protein. | Cancer and Termination of Signal Pathways .txt |
But what happens if that gene that encodes for this structure is actually mutated in some way? | Cancer and Termination of Signal Pathways .txt |
And let's suppose we mutate that gene in such a way so that this molecule loses its ability to basically hydrolyze the GTP back into GDP. | Cancer and Termination of Signal Pathways .txt |
And so if there's a mutation that takes place in the Ras gene, and the mutation basically destroys the Gtpa's activity of this g protein, then once the protein is activated, it will remain in the on position. | Cancer and Termination of Signal Pathways .txt |
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