We're back to grad student presentations this week and we have two microbiologically-oriented presentations for you.
First up is John Savopoulos. He wanted me to be sure to advertise his mug on his poster below:
Second is Stephen Muhindi:
Looking forward to seeing all of you in seminar!
This blog is devoted to BIOL 6988, a graduate level seminar in the biological sciences at Youngstown State University. While targeted towards graduate students, BIOL 6988 actively incorporates undergraduate participants in their scholastic endeavors in the biological sciences. This blog is intended as a educational tool not just for YSU students and faculty, but for anyone who wishes to contribute to an active-learning environment.
Both John and Stephen gave very interesting presentations last week, showing dedication and hard work in their research. Since we did not really have any time for questions, comments, or “compliments,” I would just like to say great job to my fellow classmates/researchers/friends.
ReplyDeleteJohn began by introducing the fungus, Neurospora crassa, belonging to the phylum Ascomycota. He spoke of its usefulness in molecular biology and gene studies (e.g. its ability to quickly grow and propagate on defined growth media). He points out that N. crassa may use different carbon sources for energy. He continued by discussing genes expressed in N. crassa with utilization of the quinic acid metabolism as the sole carbon source (a poor carbon source), specifically looking at glycogen phosphorylase, peptidyl-prolyl cis-trans isomerase, and woronin body major protein (Hex-1). Out of the three genes, woronin body protein proved to be the most interesting, having elevated expression to quinic acid metabolism and having suppressed expression to starvation. These results led to the conclusion that this was a response to the quinic acid gene cluster while glycogen phosphorylase, on the other hand, did not seem related as it did not show an elevated response to quinic acid metabolism and peptidyl-prolyl isomerase showed elevation with starvation.
Stephen then followed up with an intriguing presentation on the cloning and sequencing of mercury resistance genes from Enterobacter sp. YSU and Stenotrophomonas maltophilia OR02. Stephen thoroughly introduced mercury, its different forms, effects, and values. He continued to familiarize mercury resistant proteins and their function. Expression levels of mercury resistance were analyzed for both strains and ultimately showed S. maltophilia to be more resistant between the two strains. Do you believe this is related to a higher expression of merA?
I would also like to say that both Stephen and John gave wonderful presentations!
ReplyDeleteWhile I also work with S. maltophilia, its mechanism of mercury resistance is not my area of expertise. I would have to say that its heightened resistance in comparison with Enterobacter sp. YSU probably is due to higher expression of merA as Carmen suggested. However it is possible that the S. maltophilia strain also possesses other mechanisms to aid in resistance that the YSU Enterobacter strain may not possess.
The S. malt strain is highly resistant to quite a few metals (as well as antibiotics) so its easy to think that there are probably quite a few mechanisms working in its favor.
John and Stephen showcased yet more fine examples of the research that goes on here in the YSU Biological Sciences department. Our molecular group is doing some really interesting stuff, like John and Dr. Asch’s work on understanding mechanisms underlying gene expression and Stephen and Dr. Caguiat’s work identifying and sequencing metal resistance genes in bacteria. Since MERA reduces it to a volatile form, increasing MerA would probably speed up removal of mercury from the cells. So I do think that the heightened mercury resistance in the SO2 strain is due to increased MerA expression. RT-PCR could be used to measure RNA levels. If RNA levels are higher in the SO2 strain than the YSU strain, then enhanced mercury resistance could be owed to greater MerA expression.
ReplyDeleteJohn and Stephen both did awesome jobs presenting! Like Kyle said, there is plenty of interesting research happening in our department. To answer Carmen’s question, yes, I do think that increased mercury resistance in the SO2 strain is linked to the higher levels of merA expression.
ReplyDeleteI'm going with the consensus here in complimenting John and Stephen on their seminar presentations this past week. Great job guys! To answer Carmen's question, I do think it's a high possibility that merA is expressed in higher levels in S. maltophilia but it could also be possible, like Jamielynn said, that S. maltophilia is using other resistance genes at its disposal to make it have higher mercury resistance than the YSU Enterobacter.
ReplyDeleteI don't mean to be a broken record, but you two really did do an awesome job and discussed really interesting research topics! To answer the question, I also think that increased mercury resistance is associated with increase expression of merA. But, like Jamielynn and Kayla said, there could be other strain expressions that can contribute to this higher resistance.
ReplyDeleteCongrats to John and Stephen on their wonderful presentations! They both contained some really interesting research and comments. It makes sense with an increase in merA expression would lead to increased mercury resistant. However, other expressions should be investigated to see if there are any other causes for higher resistance. This could be some really interesting future work.
ReplyDeleteAwesome job to our graduate students on another awesome week of presentations. John and Stephen, you both did excellent jobs presenting your interesting research. It is great to see the level of importance the research being done at YSU will have. As for Carmen’s question, I would have to agree with everyone and say that the higher resistance was related to the higher expression of the MerA. Further research in determining what makes S. maltophilia more resistant than the YSU strain could help better understand the mechanisms of the two strands.
ReplyDeleteGood job to both John and Stephen! I do think it is related to higher expression.
ReplyDeleteFirst of all, thank you so much Carmen for scribing for these presentations.
ReplyDeleteSecondly, I really think John and Stephan both did a wonderful job presenting their research. As I am a very humancentric scientist (not very proud of it) but that is how my brain works. So, my question for john was how is quinic acid metabolizing species be helpful for humans?
Stephen and John, awesome to hear you presenting your research! Keep it up!
ReplyDeleteCarmen, I would hypothesize that the increased mercury resistance observed in S. maltophilia is due, at least in part, to the increased expression of merA. We cannot yet conclude that increased expression of merA is responsible for the entire effect, but it is surely responsible for at least some of the observed resistance.
Saher, I realize that your question was directed at John, but I’d just like to point out that oseltamivir (TAMIFLU) is synthesized from quinic acid and the two compounds share structural similarities that may include binding sites to some of the catabolic enzymes expressed by Neurospora crassa. Further, I have included this quote from the literature linked below:
“The NPs are decorated with quinic acid, a synthetic mimic of sialyl lewis-x, which binds to E-selectin, overexpressed on the surface of endothelial cells surrounding solid tumors.”
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3717395/