12 thoughts on “C57 – Lenoir

  1. Hi! I was wondering if your research took any inspiration or continued research from labs unaffiliated or affiliated with CU?

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    1. The research that showed the upregulation of WD40 during conjugation was done by another lab: Institute of Hydrobiology, Chinese Academy of Sciences (Wuhan, China)

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  2. Fantastic presentation! Knowing nothing about this topic, I was able to follow along pretty well! I did want to ask, though, if your gene expression results suggested that there was greater expression in the untreated samples (i.e. the green in the pie chart was larger than the red), what would this imply? Or is this even possible?

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    1. Thank you! I’m sure this is possible (though I don’t have any example of it), for instance I imagine this could indicate a gene involved in a non-essential process that is shut-down to prioritize DNA repair.

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  3. Hi! I though your presentation was very interesting but I have one question. Do you think this research could be taken a step further using lab rats?

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    1. Ultimately I think we’re most interested in human applications, so if the rat WD40 gene is more closely related to the human one than the T. therm one is, that could be an interesting route to take. For this type of explorative work though the easier the model organism is to work with, to a certain extent the better. But I’m sure we could use some rat cells in a culture dish for such an experiment.

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    1. for the actual experiment we only use cDNA, so that’s the important part. Because the gDNA PCR product for WD40 has a different length (it contains introns), if serves to validate the primer in a different way, leading to a higher confidence of primer validation if successful.

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  4. This was so interesting to hear about and easy to follow. I was curious to how the success of your results could be furthered, as you mentioned the ability to possibly have some cure for cancer. What further research could confirm this?

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    1. this would be much further down the line. Basically the more we understand the proteins involved in DNA repair, the more chances we have of finding cancer therapeutics.
      I see two ways this might be the case
      1) the protein we investigated is directly mutated in a form of cancer, so gene therapy or gene targeting could serve as a treatment
      2) some other drug is trying to kill a cancer cell line, but this cell line is resistant to DNA damage, we could directly attack this DNA damage repair proteins to reduce it’s DNA damage repair capabilities.

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    1. this is done using a process called RT PCR (mRNA is converted to cDNA) this part we actually weren’t involved with directly, we were tasked with analysing treated and untreated cDNA samples that were provided to us.

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