Based on your results, T. thermophilia has shown success with DNA repair and Rdn2 gene expression, did any of your research indicate that there could be a similar genetic code for gene expression in humans or another multicellular eukaryote that would exhibit similar findings?
I would predict that there are other multicellular eukaryotes that exhibit similar findings! We haven’t done work with any other organisms, but since some aspects of the genetic code like DNA damage repair pathways are broadly conserved across many different cell types, T. thermophila can inform work on other organisms (hopefully including humans!).
You mentioned the genome of T. thermophilia is similar to those of higher organisms, which could mean human cells would react in a similar way. How could this be beneficial for humans, what downstream issues could arise if human DNA repairing is not studied further?
Since DNA damage is constantly occurring, it would be fatal if the DNA damage repair pathway wasn’t working. These experiments in T. thermophila can also inform how humans undergo the DNA damage repair pathway and ultimately keep their cells alive! Like I mentioned in the presentation, T. thermophila has a broadly conserved biology, so a lot of the processes this organism undergoes are similar to humans. If we were to stop studying human DNA repair, then we wouldn’t be able to cure ailments like cancer or other diseases caused by DNA damage!
What could we do with the information that the RDN2 could be involved in T. thermophilia repairing pathway(after repeating experiments to validate this)?
Ultimately, it could mean that Rdn2 is found to be necessary in the DNA damage repair pathway. If this gene is necessary, then we can check for the presence of similar genes in humans (Rdn2 is a nucleotidyltransferase, so we could find a gene that does the same thing in humans). Then, we could test that gene with a human cell line and determine whether the same effect is seen in human cells! This would inform potential treatments for DNA damage-related diseases, because we could design a drug to upregulate this gene in humans that are having problems with DNA damage.
Because DNA repair pathways are conserved among eukaryotes and prokaryotes, this work in T. thermophila could tell us how human DNA repair pathways work! This is really important in coming up with treatments for cancer and other ailments.
Yes, DNA repair pathways occur in all cells, including prokaryotes and eukaryotes! That’s precisely why we picked T. thermophila, because the DNA repair pathways it uses could very well be similar (or identical) to the pathways that human cells use!
The process of DNA damage repair could definitely be similar in humans, and that’s why we’re studying it! These methods could probably work on a human cell line (or a cancer cell line), but those cells are much more difficult to work with, and we would need to be working in a sterile biological hood to do that. Unfortunately that is just beyond the scope of our abilities in an undergraduate course, but I’d love to study that in the future!
That is definitely possible! If we were to continue our experiments, then I would want to check that out. I predict that Rdn2 expression does increase as DNA damage increases, but I’m not sure!
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Based on your results, T. thermophilia has shown success with DNA repair and Rdn2 gene expression, did any of your research indicate that there could be a similar genetic code for gene expression in humans or another multicellular eukaryote that would exhibit similar findings?
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I would predict that there are other multicellular eukaryotes that exhibit similar findings! We haven’t done work with any other organisms, but since some aspects of the genetic code like DNA damage repair pathways are broadly conserved across many different cell types, T. thermophila can inform work on other organisms (hopefully including humans!).
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You mentioned the genome of T. thermophilia is similar to those of higher organisms, which could mean human cells would react in a similar way. How could this be beneficial for humans, what downstream issues could arise if human DNA repairing is not studied further?
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Since DNA damage is constantly occurring, it would be fatal if the DNA damage repair pathway wasn’t working. These experiments in T. thermophila can also inform how humans undergo the DNA damage repair pathway and ultimately keep their cells alive! Like I mentioned in the presentation, T. thermophila has a broadly conserved biology, so a lot of the processes this organism undergoes are similar to humans. If we were to stop studying human DNA repair, then we wouldn’t be able to cure ailments like cancer or other diseases caused by DNA damage!
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What could we do with the information that the RDN2 could be involved in T. thermophilia repairing pathway(after repeating experiments to validate this)?
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Ultimately, it could mean that Rdn2 is found to be necessary in the DNA damage repair pathway. If this gene is necessary, then we can check for the presence of similar genes in humans (Rdn2 is a nucleotidyltransferase, so we could find a gene that does the same thing in humans). Then, we could test that gene with a human cell line and determine whether the same effect is seen in human cells! This would inform potential treatments for DNA damage-related diseases, because we could design a drug to upregulate this gene in humans that are having problems with DNA damage.
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How could this help humans and modern medicine?
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Because DNA repair pathways are conserved among eukaryotes and prokaryotes, this work in T. thermophila could tell us how human DNA repair pathways work! This is really important in coming up with treatments for cancer and other ailments.
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Do you know if there’s any process of DNA repair pathways in any human cell?
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Yes, DNA repair pathways occur in all cells, including prokaryotes and eukaryotes! That’s precisely why we picked T. thermophila, because the DNA repair pathways it uses could very well be similar (or identical) to the pathways that human cells use!
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Would the process be the same with humans? Would any problems arise from using this method on humans?
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The process of DNA damage repair could definitely be similar in humans, and that’s why we’re studying it! These methods could probably work on a human cell line (or a cancer cell line), but those cells are much more difficult to work with, and we would need to be working in a sterile biological hood to do that. Unfortunately that is just beyond the scope of our abilities in an undergraduate course, but I’d love to study that in the future!
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Would the amount fo Rdn2 produce increase with the amount of DNA damage present?
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That is definitely possible! If we were to continue our experiments, then I would want to check that out. I predict that Rdn2 expression does increase as DNA damage increases, but I’m not sure!
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