ArticleNature communications2024
A fast-acting lipid checkpoint in G1 prevents mitotic defects.
Article in Nature communications, 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, 12 citations in OpenAlex.
- Pre-mRNA splicing regulates cellular dedifferentiation via lipid metabolism in a cytokinin-dependent manner in Arabidopsis.Plant physiology · 2026Article
- Integrin β3 Promotes Retinal Neovascularization via Endoplasmic Reticulum Stress-Mediated Endothelial Cell Senescence.Investigative ophthalmology & visual science · 2026Article
- High-content imaging and transcriptomic analyses of the effects of bisphenol S and alternative color developers on KGN granulosa cells.Toxicological sciences : an official journal of the Society of Toxicology · 2025Article
- Temporal oscillation of phospholipids promotes metabolic efficiency.Nature chemical biology · 2025Article
- The HDAC inhibitor romidepsin renders liver cancer vulnerable to RTK targeting and immunologically active.Nature communications · 2025Article
- Sphingolipid synthesis maintains nuclear membrane integrity and genome stability during cell division.The Journal of cell biology · 2025Article
- Cell cycle proteins: Linking the cell cycle to tumors.Oncology research · 2025Review
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Authors and funding
8 authors at 5 institutions in 1 country.
Funding
Abstract
Lipid synthesis increases during the cell cycle to ensure sufficient membrane mass, but how insufficient synthesis restricts cell-cycle entry is not understood. Here, we identify a lipid checkpoint in G1 phase of the mammalian cell cycle by using live single-cell imaging, lipidome, and transcriptome analysis of a non-transformed cell. We show that synthesis of fatty acids in G1 not only increases lipid mass but extensively shifts the lipid composition to unsaturated phospholipids and neutral lipids. Strikingly, acute lowering of lipid synthesis rapidly activates the PERK/ATF4 endoplasmic reticulum (ER) stress pathway that blocks cell-cycle entry by increasing p21 levels, decreasing Cyclin D levels, and suppressing Retinoblastoma protein phosphorylation. Together, our study identifies a rapid anticipatory ER lipid checkpoint in G1 that prevents cells from starting the cell cycle as long as lipid synthesis is low, thereby preventing mitotic defects, which are triggered by low lipid synthesis much later in mitosis.
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Registered trials
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