CHARACTERISATION OF RICTOR’S ROLE IN Caenorhabditis elegans

Abstract

Dietary flexibility is crucial for an organism's survival, yet the molecular mechanisms governing this adaptation and its impact on aging remain poorly understood. Our findings shed light on the multifaceted role of RICTOR, a key component of the mTOR signaling pathway, in modulating stress responses, mitophagy, and longevity using C. elegans as a model organism. We first demonstrate that rict-1 mutants exhibit enhanced osmotic stress tolerance, particularly when fed an HT115 diet, implicating mTORC2 signaling in stress response regulation. Then we looked at the role of RICTOR in mitochondrial homeostasis. The lack of significant changes in hsp-60 expression challenges us to understand mitochondrial unfolded protein response (UPRmt) as a cellular mechanism underlying stress responses. Moreover, investigation of mitophagy markers including PINK-1 expression reveals intriguing insights into mitochondrial quality control mechanisms. Further, we got interested in understanding the relation between lipid metabolism and collagen biosynthesis. We observe elevated lipid accumulation in rict-1(ft7), particularly on an OP50 diet. These findings underscore the importance of RICTOR in regulating fat metabolism and ECM dynamics. Lastly, our lifespan analysis highlights the critical roles of pink-1 and pdr-1, in regulating longevity in rict-1 mutants, further emphasizing the importance of mitochondrial quality control pathways in aging.