Phosphatidylcholine acyl turnover facilitates thylakoid lipid remodeling and promotes plant survival under heat stress

Summary Heat stress destabilizes chloroplast membranes, requiring rapid lipid remodeling to maintain photosynthetic function. Although thylakoid lipid remodeling and triacylglycerol (TAG) accumulation are established heat responses, the role of phosphatidylcholine (PC) acyl turnover remains unclear. We investigated lysophosphatidylcholine acyltransferase 1 and 2 (LPCAT1/2), REDUCED OLEATE DESATURATION1 (ROD1), phospholipid:diacylglycerol acyltransferase 1 (PDAT1), and lipins in heat‐induced lipid remodeling and thermotolerance in Arabidopsis thaliana . Using genetic, lipidomic, physiological, and photosynthetic analyses, we examined mutants defective in PC acyl editing, PC–diacylglycerol (DAG) interconversion, TAG synthesis, and phosphatidic acid dephosphorylation during heat stress. Loss of LPCAT1/2 severely impaired basal and acquired thermotolerance, caused irreversible photosystem II damage, and disrupted thylakoid lipid remodeling. rod1 showed minor defects, whereas rod1 lpcat1/2 exhibited enhanced thermosensitivity. In mature vegetative plants, pdat1‐2 showed thermotolerance and photosystem II defects comparable to lpcat1/2 . Lipin‐mediated phosphatidic acid dephosphorylation provided the major DAG source for heat‐induced TAG synthesis. Defective PC acyl turnover also increased free fatty acids and lipid peroxidation. These findings establish LPCAT1/2‐mediated PC acyl turnover as a central regulator of heat‐induced membrane remodeling and thermotolerance and link lipin‐dependent DAG production and TAG synthesis with chloroplast membrane homeostasis.