Ibiagbani Max-Harry
The Molecular and Cellular Biology Seminar series features Ibiagbani Max-Harry discussing “I’m Aging, What’s to Blame? The Role of the Gut Microbiota and Autophagy in Longevity” on April 13 from 4:35 – 5:55 p.m.
- Contact Dr. Sarah Wyatt, MCB director, for Teams information.
Max-Harry is a graduate student in Biological Sciences at Ohio University and a member of the Molecular and Cellular Biology program.
Abstract: The causes of aging and possible interventions to slow down the process have be-come major areas of research in recent years. Activation of the self-eating process, autophagy, where damaged cells, organelles and proteins are gotten rid of through lysosomal engulfment has been shown to slow down aging in mice (1). The mamma-lian target of Rapamycin complex (mTORc) is activated in the presence of nutrients and is known to suppress autophagy by inhibiting ULK1, a key autophagy inducer. Various studies show that nutrient deprivation enhances autophagy and longevity in both mice and flies. Rapamycin is a chemical compound which inhibits mTORc1 and has been shown to increase lifespan, slow down age-related disorders such as changes in the gut microbiota in different model organisms. Schinaman et al showed that although administering rapamycin affected the gut microbiota of Drosophila, it also slowed down aging in “germ-free” flies with no gut microbiota (2). They further showed that knocking out the autophagy related gene ATG1 prevented rapamycin mediated longevity. These results reveal that although modified by rapamycin, the gut microbiota, unlike autophagy, is not required for rapamycin action. Further stud-ies are needed to understand if a relationship exists between autophagy and the gut microbiota composition.
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