ArticleThe Journal of cell biology2022
mTORC2 suppresses cell death induced by hypo-osmotic stress by promoting sphingomyelin transport.
Article in The Journal of cell biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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Who cites it
7 citing papers in PubMed, 8 citations in OpenAlex.
- Article
- Functional profiling and visualization of the sphingolipid metabolic network in vivo.EMBO reports · 2025Article
- A dynamic feedback loop between retrograde sterol transport and TORC2 controls adaptation of the plasma membrane to stress.The EMBO journal · 2025Article
- A steady-state pool of calcium-dependent actin is maintained by Homer and controls epithelial mechanosensation.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- CRISPRi screening identifies PIKfyve as a co-therapeutic target for obinutuzumab.Clinical and translational medicine · 2025Article
- Making PI3K superfamily enzymes run faster.Advances in biological regulation · 2025Review
- The mTORC2 signaling network: targets and cross-talks.The Biochemical journal · 2024Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epithelial cells are constantly exposed to osmotic stress. The influx of water molecules into the cell in a hypo-osmotic environment increases plasma membrane tension as it rapidly expands. Therefore, the plasma membrane must be supplied with membrane lipids since expansion beyond its elastic limit will cause the cell to rupture. However, the molecular mechanism to maintain a constant plasma membrane tension is not known. In this study, we found that the apical membrane selectively expands when epithelial cells are exposed to hypo-osmotic stress. This requires the activation of mTORC2, which enhances the transport of secretory vesicles containing sphingomyelin, the major lipid of the apical membrane. We further show that the mTORC2-Rab35 axis plays an essential role in the defense against hypotonic stress by promoting the degradation of the actin cortex through the up-regulation of PI(4,5)P2 metabolism, which facilitates the apical tethering of sphingomyelin-loaded vesicles to relieve plasma membrane tension.
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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.