ArticleCommunications biology2024
Mobilization of cholesterol induces the transition from quiescence to growth in Caenorhabditis elegans through steroid hormone and mTOR signaling.
Article in Communications biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 13 citations in OpenAlex.
- Bacterial-derived cyclic lipopeptides suppress dauer arrest inbioRxiv : the preprint server for biology · 2026Article
- Developmental plasticity enables an intestinal tapeworm to adapt to dietary stress.Nature communications · 2026Article
- Starve-Feed Cycles Direct Quiescence to Proliferation Transitions inbioRxiv : the preprint server for biology · 2026Article
- AMPK modulates a DEAH box RNA-helicase to attenuate TOR signaling and establish developmental quiescence in Caenorhabditis elegans.PLoS biology · 2025Article
- From Worms to Tumors: Conserved Strategies of Cellular Arrest and Survival Governing Dormancy.Cancer research · 2025Review
- The C. elegans LON-1 protein requires its CAP domain for function in regulating body size and BMP signaling.Genetics · 2025Article
- The transcriptome of early compensatory kidney growth reveals cell and time specific responses.iScience · 2024Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recovery from the quiescent developmental stage called dauer is an essential process in C. elegans and provides an excellent model to understand how metabolic transitions contribute to developmental plasticity. Here we show that cholesterol bound to the small secreted proteins SCL-12 or SCL-13 is sequestered in the gut lumen during the dauer state. Upon recovery from dauer, bound cholesterol undergoes endocytosis into lysosomes of intestinal cells, where SCL-12 and SCL-13 are degraded and cholesterol is released. Free cholesterol activates mTORC1 and is used for the production of dafachronic acids. This leads to promotion of protein synthesis and growth, and a metabolic switch at the transcriptional level. Thus, mobilization of sequestered cholesterol stores is the key event for transition from quiescence to growth, and cholesterol is the major signaling molecule in this process.
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Registered trials
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