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Academic background:

Post Graduation: M.Sc. (Zoology) (The M. S. University of Baroda)

 

Theme for my current research work:

Cellular senescence is the arrest of the cell cycle along with the secretion of certain factors (known as senescence-associated secretory phenotype, SASP) that can alter its microenvironment and impact the overall tissue. Cellular senescence is characterized by hypertrophy, increased ROS, DNA damage, mitochondrial dysfunction, and an increased lysosomal β Gal activity. This phenomenon is essential for various processes like fetal development, wound healing, tissue remodeling, and maintaining tissue homeostasis. However, when cellular senescence goes in the toss, it often leads to chronic conditions like cancer, immune disorders, cardiac diseases, and neurodegenerative diseases. Interestingly, senescence displays two opposing, context-dependent associations with diseases such as cancers. Deciphering these senescence-linked disease promotions or inhibition requires examination of the causally associated genetic circuitries in a genetically highly tractable model organism like Drosophila. Toward these goals, we are exploring Drosophila organs that are likely ideal for probing these questions. We have seen that the adult male accessory organ (MAG) represents one such organ. The squamous epithelial lining of the fluid-filled lumen of Drosophila adult MAG displays age-related changes in its tissue architecture, a loss of its tricellular junctional integrity being one such. Thus, we aim to present evidence of the utility of the adult MAG in modeling an entire gamut of senescence-linked human diseases in Drosophila and uncovering their mechanistic underpinnings.

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Drosophila Male Accessory gland (MAG) displaying its cellular architecture. 

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