ArticleCell metabolism2011
Phosphatidylcholine synthesis for lipid droplet expansion is mediated by localized activation of CTP:phosphocholine cytidylyltransferase.
Article in Cell metabolism, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 286 papers.
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Who cites it
286 citing papers in PubMed, 529 citations in OpenAlex.
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- Sphingosine kinase-2 inhibition promotes immunogenic differentiation of myeloid-derived suppressor cells through an Acetyl-CoA carboxylase-phosphatidylcholine axis.Nature communications · 2026Article
- Heterogeneity, dynamics and organelle interactions of lipid droplets.Nature reviews. Molecular cell biology · 2026Review
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- Decoding color variation: genome-wide characterization and expression analysis of pigment pathways in Neocaridina denticulata.BMC genomics · 2026Article
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- Emerging complexities of phospholipid metabolism in adipose tissue.Molecules and cells · 2026Review
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- Feeding Diqing Tibetan pigs with 50% of soybean meal replaced by walnut meal can reduce subcutaneous fat deposition and promote intramuscular fat accumulation.Frontiers in microbiology · 2026Article
- Sec14L6 is a phosphoinositide transporter that regulates phosphoinositide homeostasis and biogenesis of lipid droplets.Nature communications · 2025Article
- Navigating lipid droplet proteins - part II: molecular mechanisms underlying ER-to-lipid droplet protein partitioning.Biochemical Society transactions · 2025Review
- Decoding the Lipid Droplet Proteome: New Frontiers in Cardiovascular Disease Research.International journal of molecular sciences · 2025Review
226 more citing papers are in PubMed but not listed here.
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Authors and funding
12 authors at 5 institutions in 3 countries.
Funding
Abstract
Lipid droplets (LDs) are cellular storage organelles for neutral lipids that vary in size and abundance according to cellular needs. Physiological conditions that promote lipid storage rapidly and markedly increase LD volume and surface. How the need for surface phospholipids is sensed and balanced during this process is unknown. Here, we show that phosphatidylcholine (PC) acts as a surfactant to prevent LD coalescence, which otherwise yields large, lipolysis-resistant LDs and triglyceride (TG) accumulation. The need for additional PC to coat the enlarging surface during LD expansion is provided by the Kennedy pathway, which is activated by reversible targeting of the rate-limiting enzyme, CTP:phosphocholine cytidylyltransferase (CCT), to growing LD surfaces. The requirement, targeting, and activation of CCT to growing LDs were similar in cells of Drosophila and mice. Our results reveal a mechanism to maintain PC homeostasis at the expanding LD monolayer through targeted activation of a key PC synthesis enzyme.
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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.