bioRxiv Science⌕ Search

Biology subjects

Cohen-Abeles, L.

Publications and source records attributed to Cohen-Abeles, L..

2 recordsLinked to original sources

Cryo-EM structures reveal the mechanism of phosphatidylserine remodeling by membrane-bound glycerophospholipid O-acyltransferase 1

Lands cycle remodeling of glycerophospholipid acyl chains is crucial for cells to maintain appropriate membrane composition. Glycerophospholipids are cleaved at the glycerol sn2-position by phospholipase A. The lysophospholipids are reacylated by enzymes of the membrane-bound O-acyltransferase (MBOAT) family to incorporate specific fatty-acyl chains to adjust membrane properties. How MBOAT enzymes recognize specific acyl-CoA donors, select lysophospholipid acceptors, and release products is unclear. Phosphatidylserine (PS), a critical anionic phospholipid, controls membrane surface charge, signaling-protein recruitment, and cell-death-associated membrane recognition, and PS acyl-chain remodeling is linked to ferroptosis resistance. Here, we showed that MBOAT1 preferentially generates monounsaturated fatty acid-containing PS from lyso-PS. High-resolution cryo-electron microscopy structures of human MBOAT1 captured distinct binding poses of the fatty acyl donor, lyso-PS acceptor, and PS product. With lipidomics, enzymology and molecular dynamics simulations, these structures reveal the mechanism and pathway of MBOAT1-dependent PS remodeling.

biochemistry↗

A membrane homeostatic response to lipid overload coordinates fatty acid metabolism

Excess fatty acids can disrupt membrane and organelle function. Cells buffer fatty acid toxicity by synthesizing and storing triglycerides (TGs) in lipid droplets, but their capacity for TG storage is limited. Here, we impaired TG synthesis in hepatocytes and identified adaptive pathways that restore homeostasis during lipid overload. Transcription responds by activating fatty acid oxidation through peroxisome proliferator-activated receptors, and by suppressing synthesis of new, unsaturated fatty acids through sterol regulatory element-binding protein 1 (SREBP1). Mechanistically, SREBP1 appears to respond to changes in ER membrane fluidity. These findings reveal a homeostatic system monitoring and maintaining the ER membrane, coordinating fatty acid synthesis and oxidation, a finding with broad implications for understanding lipid physiology and developing TG synthesis inhibitors for treating fatty liver disease.

cell biology↗