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Reduced Translation as the key for longevity

Arvind kumar sharma Sep 04, 2020

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Mitochondrial dysregulation has always been considered as one of the many reasons for aging . But what if I tell you we can use it to prolong lifespan , just like Thanos said "I used the stones to destroy the stones", well it seems a distant reality but it has already been proved in mutants of C.elegans. The underlying hypothesis is that inhibiting cyc-2.1 (cytochrome) [1] in germline significantly extends lifespan by activating UPRmt and AMPK pathways. 

Scientific analysis using translational profiling, scientists have identified that an RNA-binding protein GLD-1 acts as a key translational repressor of cyc-2.1 [2]. Thus using RNA interference technique on C.elegans mutant daf-2 rsks-1 [3]suppressed cyc-2.1 expression by inhibiting GLD-1 which is an critical transcriptional regulators of UPRmt . Thus, a cascade of signalling follows in which the insulin-like signaling and TOR pathway-mediates an tissue-specific translational repression of cytochrome c which induces the cell for an non-autonomous mitochondrial stress response that promotes longevity. 
Imagine if we are able to reproduce the similar results in humans, as well!!!

[1]Germline Signaling Mediates the Synergistically Prolonged Longevity Produced by Double Mutations in daf-2 and rsks-1 in C. elegans doi: 10.1016/j.celrep.2013.11.018

[2]2. Jianfeng Lan, Translational Regulation of Non-autonomous Mitochondrial Stress Response Promotes Longevity doi: https://doi.org/10.1016/j.celrep.2019.06.078

[3]ClpP Mediates Activation of a Mitochondrial Unfolded Protein Response in C. elegans

longevity