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Mobilization of cholesterol induces the transition from quiescence to growth in Caenorhabditis elegans through steroid hormone and mTOR signaling.

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Schmeisser,  Kathrin
Max Planck Institute for Molecular Cell Biology and Genetics, Max Planck Society;

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Kaptan,  Damla
Max Planck Institute for Molecular Cell Biology and Genetics, Max Planck Society;

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Raghuraman,  Bharath Kumar
Max Planck Institute for Molecular Cell Biology and Genetics, Max Planck Society;

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Shevchenko,  Andrej
Max Planck Institute for Molecular Cell Biology and Genetics, Max Planck Society;

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Rodenfels,  Jonathan
Max Planck Institute for Molecular Cell Biology and Genetics, Max Planck Society;

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Penkov,  Sider
Max Planck Institute for Molecular Cell Biology and Genetics, Max Planck Society;

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Kurzchalia,  Teymuras V.
Max Planck Institute for Molecular Cell Biology and Genetics, Max Planck Society;

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Citation

Schmeisser, K., Kaptan, D., Raghuraman, B. K., Shevchenko, A., Rodenfels, J., Penkov, S., et al. (2024). Mobilization of cholesterol induces the transition from quiescence to growth in Caenorhabditis elegans through steroid hormone and mTOR signaling. Communications biology, 7(1): 121. doi:10.1038/s42003-024-05804-7.


Cite as: https://hdl.handle.net/21.11116/0000-000F-15E2-A
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.