期刊
ELIFE
卷 10, 期 -, 页码 -出版社
ELIFE SCIENCES PUBLICATIONS LTD
DOI: 10.7554/eLife.66768
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资金
- Bundesministerium fur Bildung und Forschung [0315893A]
- Deutscher Akademischer Austauschdienst [57518567]
- Max-Planck-Gesellschaft
- Fundacao de Amparo a Pesquisa do Estado de Sao Paulo [2019/25958-9]
- Coordenacao de Aperfeicoamento de Pessoal de Nivel Superior [88881.143924/2017-01]
This study reveals that miR-1 in Caenorhabditis elegans plays a role in muscle function by regulating vacuolar ATPase subunits and lysosomal biogenesis, impacting muscle function and health by coordinating lysosomal v-ATPase and biogenesis. Deletion of mir-1 can improve mid-life muscle motility, pharyngeal pumping, and organismal longevity.
Muscle function relies on the precise architecture of dynamic contractile elements, which must be fine-tuned to maintain motility throughout life. Muscle is also plastic, and remodeled in response to stress, growth, neural and metabolic inputs. The conserved muscle-enriched microRNA, miR-1, regulates distinct aspects of muscle development, but whether it plays a role during aging is unknown. Here we investigated Caenorhabditis elegans miR-1 in muscle function in response to proteostatic stress. mir-1 deletion improved mid-life muscle motility, pharyngeal pumping, and organismal longevity upon polyQ35 proteotoxic challenge. We identified multiple vacuolar ATPase subunits as subject to miR-1 control, and the regulatory subunit vha-13/ATP6V1A as a direct target downregulated via its 30 UTR to mediate miR-1 physiology. miR-1 further regulates nuclear localization of lysosomal biogenesis factor HLH-30/TFEB and lysosomal acidification. Our studies reveal that miR-1 coordinately regulates lysosomal v-ATPase and biogenesis to impact muscle function and health during aging.
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