ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2015
The integrin-adhesome is required to maintain muscle structure, mitochondrial ATP production, and movement forces in Caenorhabditis elegans.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.
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Who cites it
29 citing papers in PubMed, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.
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- A C. elegans genome-wide RNAi screen for altered levamisole sensitivity identifies genes required for muscle function.G3 (Bethesda, Md.) · 2021Article
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- Transcriptional adaptation ineLife · 2020Article
- Pluronic gel-based burrowing assay for rapid assessment of neuromuscular health in C. elegans.Scientific reports · 2019Article
- TheGenome research · 2019Article
- Disruption of mitochondrial dynamics affects behaviour and lifespan in Caenorhabditis elegans.Cellular and molecular life sciences : CMLS · 2019Article
- Muscle strength deficiency and mitochondrial dysfunction in a muscular dystrophy model ofDisease models & mechanisms · 2018Article
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Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
Abstract
The integrin-adhesome network, which contains >150 proteins, is mechano-transducing and located at discreet positions along the cell-cell and cell-extracellular matrix interface. A small subset of the integrin-adhesome is known to maintain normal muscle morphology. However, the importance of the entire adhesome for muscle structure and function is unknown. We used RNA interference to knock down 113 putative Caenorhabditis elegans homologs constituting most of the mammalian adhesome and 48 proteins known to localize to attachment sites in C. elegans muscle. In both cases, we found >90% of components were required for normal muscle mitochondrial structure and/or proteostasis vs. empty vector controls. Approximately half of these, mainly proteins that physically interact with each other, were also required for normal sarcomere and/or adhesome structure. Next we confirmed that the dystrophy observed in adhesome mutants associates with impaired maximal mitochondrial ATP production (P < 0.01), as well as reduced probability distribution of muscle movement forces compared with wild-type animals. Our results show that the integrin-adhesome network as a whole is required for maintaining both muscle structure and function and extend the current understanding of the full complexities of the functional adhesome in vivo.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.