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14 thoughts on “C23 – Moore”
Could you explain conjugation a little more?
Conjugation is when the Tetrahymena replicate. They undergo a process that gives them genetic diversity and that ultimately ends with more Tetrahymena.
How are sure of what your PCR results would have shown if the DNA had been isolated?
I’m not entirely sure but based on my hypothesis I think that Hymelc should have been increased. As for Rad51 and Ftt18, those genes have been studied previously and the gene products and expression levels are known in response to DNA damage.
Good presentation! Do you know a way to determine what pathways the gene Hymelc participates in?
This would be very similar to developmental experiments which I’m no expert in but using a different range of inhibitors and activators and many different antibodies to measure expression of different gene products you can do a sequence of experiments to place genes within a pathway. We can also do experiments to see if Hymelc binds to other proteins by using antibodies once they are able to interact with each other.
Great presentation, Can’t wait to see you in class tomorrow. How does Hydroxyurea cause DNA damage?
That’s a great question, Logan. I’m not sure how hydroxyurea causes DNA damage but I can see how it could have something to do with interrupting the phosphodiester bond between bases as it creates DSB.
Great presentation! Can you predict to what extent how significant Hymelc is in DNA damage repair?
Unfortunately without the data from the RT-PCR I cannot make any predictions. It could really be any amount of increase and there is no way to know unless we do these experiments.
What is conjugation and what role does it play in this experiment?
Conjugation is when Tetrahymena undergo replication. They spend time to increase their genetic diversity via DNA damage and then it ultimately ends with more cells.
If there is increase in expressivity of DSB repairs, will this impact normally functioning cells?
The biggest influence of DSBs on the cells is the fact that NHEJ is inherently mutagenic and in general DSBs are very difficult to repair well. This will definitely mess up many functions in the cell. If you are asking about the function of the DSB repair pathway in cells that have no or low DSBs then I think that the increased presence of these proteins will not have a deleterious affects on the cell as they are specifically recruited to DSBs and all other times are inactive.