Friday, March 10, 2017

My Turn (maybe?)


http://cmr.asm.org/content/19/1/95/F3.large.jpg

If the Trump administration permits me to return to the U.S. following my trip to China, I will be presenting seminar on March 24th.  I will be recapping my laboratory's work with Talaromyces marneffei and the role of a particular signaling factor, YakA, in the growth and development of this pathogenic fungus.  I'm positive that this will be a spell-binding lecture!  The choice of a pillow or caffeine is up to you.

8 comments:

  1. Titin is the largest polypeptide and is found in high concentration in heart and skeletal muscle. It is encoded by TNN gene and expressed in multiple isoforms because of alternative splicing. Connecting the Z line to the M line in the sarcomere, it play an important role contraction of striated muscles and contributes to force transmission at the Z line and resting tension in the I band region. It is entirely responsible for passive force generated by muscles as it limits the range of motion of the sarcomere in tension. Besides, Titin helps in organizing of the thick and thin filaments during sarcomere assembly. It also contains protein kinase domains responsible for muscle gene expression. A case study cited by Dr walker was the rippling muscle, a malfunction associated with this particular Titin domain. In his presentation Dr Walker also used sequence homology the exists in the Titin polypeptide of different organisms including Clytia hemispaeric (jelly fish) and Dosophilia to advance an augment that Titin has been evolving for the past 4 million years.
    Question:
    How has alternative splicing and point mutation contributed in evolution of Titin polypeptide

    ReplyDelete
  2. Dr. Cooper had an interesting presentation on the dimorphic fungi, T. marneffei. In an attempt to study the genes that regulate the transition from the mold phase (spore bearing) to the yeast phase (pathogenic form), a mutant was generated by randomly introducing a segment of tDNA into the genome. This resulted in the interruption of a putative yakA gene, which encodes a protein kinase (phosphorylation). After subsequent experiments, the yakA gene was determined to regulate genes that regulate glucan synthesis. This was confirmed by the increased production of chitin in the mutant which lacked proper glucan synthesis, compared to the wildtype and the genetic complement which had a functioning yakA gene. Based on the background reading, yakA appears to have a response to increased temperatures.
    How could a defect in the cell wall due to the decrease in glucan synthesis be effected by increased temperatures (such as a fever)?

    ReplyDelete
  3. Dr. Cooper's presentation was very insightful. It was interesting to learn about the yakA gene, which regulates glucan synthesis. I had heard about this gene before, but I was not aware that it influenced the production of chitin. Dr. Cooper did a great job of explaining all genes and species used in the study.

    ReplyDelete
  4. A couple of summers ago I had a chance to work at Dr Coopers lab , and gained more in depth knowledge about what's going on in his lab and techniques employed during the research. Dr Cooper mentioned that they compared wild type to the mutant, and they found that mutant germinates faster at 25C and 37C when compared to wild type. I don't think it will be effected, since fever is considered to be around 39-41C i don't think temperature would have a severe effect on the cell

    ReplyDelete
  5. Like Amina, I have heard of the yakA gene before and was also unaware of it's influence on chitin production. After doing a bit of research, it appears that disruption of the gene causes perturbation of the cell wall. Increases in temperature can cause further degradation of cells. But because the mutant type flourishes at higher temperatures, I believe that an increase in temperature, such as fever, would promote cell growth.

    ReplyDelete
  6. As Jameaka states, denaturation in DNA due to temperature increases can affect how these cells reproduce or how different genes in the cell are regulated (over or under) and not necessarily making them not functionable.. Some studies have showed that P. marneffei may have certain ways of regulating their genes at the higher temperatures.

    ReplyDelete
  7. Adding onto what Ludmila said above, it's been shown that P. marneffei increases its tandem repeat sequences at higher temperatures. I'm not entirely sure whether an increasing in coding for tandem repeats would push out more important coding regions or not, but I think it would be an interesting topic to investigate.

    ReplyDelete
  8. Studies have shown that yakA in P. marneffei is important in not only in conidiogenesis, but also in germination and cell wall integrity. There is also evidence indicating that the yakA gene is involved in response to heat shock stress in yeast development. The kinase encoded by yakA appear to play an important role in the regulation of chitin synthesis and its deposition as cell wall component. Although it is not clearly understood how exactly yakA exerts these effects, It is believed that the abnormal synthesis and deposition of chitin is a reaction to aberrations in the hyphal cell wall.

    ReplyDelete