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Unveiling the tissue-specific contribution of ALG-1 for oxidative stress response of C. elegans

Grant number: 21/13222-8
Support Opportunities:Scholarships abroad - Research Internship - Doctorate (Direct)
Effective date (Start): May 06, 2022
Effective date (End): April 30, 2023
Field of knowledge:Biological Sciences - Biochemistry - Molecular Biology
Principal Investigator:Marcelo Alves da Silva Mori
Grantee:Carlos Alberto Vergani Junior
Supervisor: William Mair
Host Institution: Instituto de Biologia (IB). Universidade Estadual de Campinas (UNICAMP). Campinas , SP, Brazil
Research place: Harvard University, Cambridge, United States  
Associated to the scholarship:19/01587-1 - Study of the role of ALG-1 and its regulatory mechanisms in healthspan of Caenorhabditis elegans, BP.DD


Population aging represents a relevant public health issue, justifying the pursue of interventions aiming to promote health in the elderly. In the aging process, cells tend to lose the ability to properly respond to endogenous and exogenous stressors, and one relevant stress related to aging is oxidative stress. High levels of pro-oxidant molecules associated with decreased antioxidant capacity may result in oxidative stress, which in turn, may culminate in cell death or dysfunction. miRNAs and components of miRNA biogenesis modulate pathways implicated in longevity and stress response. In my PhD project, we have shown that alg-1 knockdown in C. elegans decreases resistance to oxidative stress promoted by sodium arsenite or methyl viologen (paraquat). Moreover, ALG-1 overexpression (ALG- 1 O/E) leads to a greater resistance against these pro-oxidant agents. Although our results indicate that ALG-1 is both necessary and sufficient to promote resistance to oxidative stress, the specific mechanisms by which ALG-1 controls oxidative stress response still need to be elucidated. One way to understand more about how ALG-1 overexpression benefits health is investigating in which tissue(s) it acts to confer stress resistance at the whole organism level. For that, in this project, we propose to investigate the tissue-specific contribution of ALG-1 and a few miRNAs known to be upregulated when ALG-1 is overexpressed. Using genetic tools available or developed at the Mair lab, we will generate C. elegans strains that will allow us to inhibit or rescue ALG-1 and miRNAs in specific tissues. We will then test how these strains resist pro-oxidant agents and what are the tissue specific targets of the miRNAs that could allow worms to control redox balance. Thus, we hope to elucidate the contribution of ALG-1 and specific miRNAs for the oxidative stress response in specific tissues and provide new mechanistic insights regarding the regulation of redox balance from cell to the organismal level. (AU)

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