This Friday, March 19th, Ms. Patricia Chemutai will present her current research being conducted with Dr. Gary Walker entitled "GENE EXPRESSION IN LONG TERM MYOBLAST/MYOCYTE CULTURES: m RNA expression (AChR & Gal-3)".
Please actively participate in this seminar presentation.
Bravo! Patricia's presentation gave great background information on how muscle contraction is initiated. She then transitioned into her research on the different levels of expression in the Gal-3 and AChR genes at different points in myocyte aging and repair. After seeing the methods and results, a couple of questions arose. So, my question to you...How do you think a mutation in the Gal-3 gene that causes lower levels of expression may affect muscle repair?
ReplyDeletePatricia did a great job. Gal-3 functions both intracellularly through protein-protein interactions and extracellularly by binding specific glycans on glycoproteins. Gal-3 is expressed in muscles which are required to initiate muscle repair. It binds to its ligands forming crosslinks which results in cell-cell adhesion, cell-matrix interactions, signal transduction, membrane receptor dynamics, and cell mobility which are all necessary in myogenesis (muscle regeneration/repair). Gal-3 also increases the biosynthesis and expression of the glycan ligands of Gal-3 which increases the efficiency of myogenesis. It also facilitates the intimate interactions of differentiating myoblasts that promote myogenesis. Gal-3 is one of the laminin-binding proteins and its binding enhance cell adhesion to the basal lamina. Mutations at different binding sites of Gal-3 prevents ability of Gal-3 to bind to the glycan-ligands thus affecting all the activities I mentioned above of gal-3 in muscle repair.
ReplyDeletePatricial gave a phenominal presentation of her research! As for mutations in the Gal-3 gene that affect expression levels, I'd say that Annah summed up my thoughts on possible effects of Gal-3 mutations. Assuming that there is no other gene that a similar role, or if there is but does not fulfill the role as efficiently, I would imagine that mutations in gene products that are involved in several cellular processes and interactions, like Gal-3, are bound to show some adverse affect.
ReplyDeleteVery informative presentation! On a genetics level, I wonder if Gal-3 can be edited to be upregulated again as an individual gets older. Perhaps the fountain of youth isn't so far away
ReplyDeleteSince high expression of Gal-3 is required for muscle repair, mutation will bring about decrease in expression of Gal-3 thus the integrity of muscle mass is disrupted.
ReplyDeletePatricia gave a great presentation on her research of muscles and AChR and Gal-3. Annah covered all of the bases in answering the posed question on the possible Gal-3 mutations. I question the opposite, what if there is an overexpression of Gal-3. Could this be a possible way to better repair muscle? Could athletes with an over expression workout multiple times a day with no adverse issues? Could the muscle repair itself quicker and improve recovery time leading to a “superhuman” scenario? If so, I would like to be the first one in line for the experimental treatment.
ReplyDeleteWow I love all of these comments. Patricia did a great job presenting clearly and focused. Annah did sum up the question but for Dakotas questions sometimes there is too much of a good thing that could make it bad... if you keep growing muscle then eventually it could be too much too fast and start impacting other capabilities in the body. Just an opinion but good question.
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