An Intricate Network Involving the Argonaute ALG-1 Modulates Organismal Resistance to Oxidative Stress

Carlos A. Vergani-Junior, Raíssa De P. Moro, Silas Pinto, Evandro A. De-Souza, Henrique Camara, Deisi L. Braga, Guilherme Tonon-da-Silva, Thiago L. Knittel, Gabriel P. Ruiz, Raissa G. Ludwig, Katlin B. Massirer, William B. Mair and Marcelo A. Mori ()
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Carlos A. Vergani-Junior: Universidade Estadual de Campinas
Raíssa De P. Moro: Universidade Estadual de Campinas
Silas Pinto: Universidade Estadual de Campinas
Evandro A. De-Souza: Universidade Estadual de Campinas
Henrique Camara: Universidade Estadual de Campinas
Deisi L. Braga: Universidade Estadual de Campinas
Guilherme Tonon-da-Silva: Universidade Estadual de Campinas
Thiago L. Knittel: Universidade Estadual de Campinas
Gabriel P. Ruiz: Universidade Estadual de Campinas
Raissa G. Ludwig: Universidade Estadual de Campinas
Katlin B. Massirer: Universidade Estadual de Campinas
William B. Mair: Harvard University
Marcelo A. Mori: Universidade Estadual de Campinas

Nature Communications, 2024, vol. 15, issue 1, 1-15

Abstract: Abstract Cellular response to redox imbalance is crucial for organismal health. microRNAs are implicated in stress responses. ALG-1, the C. elegans ortholog of human AGO2, plays an essential role in microRNA processing and function. Here we investigated the mechanisms governing ALG-1 expression in C. elegans and the players controlling lifespan and stress resistance downstream of ALG-1. We show that upregulation of ALG-1 is a shared feature in conditions linked to increased longevity (e.g., germline-deficient glp-1 mutants). ALG-1 knockdown reduces lifespan and oxidative stress resistance, while overexpression enhances survival against pro-oxidant agents but not heat or reductive stress. R02D3.7 represses alg-1 expression, impacting oxidative stress resistance at least in part via ALG-1. microRNAs upregulated in glp-1 mutants (miR-87-3p, miR-230-3p, and miR-235-3p) can target genes in the protein disulfide isomerase pathway and protect against oxidative stress. This study unveils a tightly regulated network involving transcription factors and microRNAs which controls organisms’ ability to withstand oxidative stress.

Date: 2024
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DOI: 10.1038/s41467-024-47306-4

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