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Head group-acylated chloroplast lipids were discovered in the 1960s, but interest was renewed about 15 years ago with the discovery of Arabidopsides E and G, acylated monogalactosyldiacylglycerols with oxidized fatty acyl chains originally identified in Arabidopsis thaliana . Since then, plant biologists have applied the power of mass spectrometry to identify additional oxidized and non-oxidized chloroplast lipids and quantify their levels in response to biotic and abiotic stresses. The enzyme responsible for the head-group acylation of chloroplast lipids was identified as a cytosolic protein closely associated with the chloroplast outer membrane and christened acylated galactolipid-associated phospholipase 1 (AGAP1). Despite many advances, critical questions remain about the biological functions of AGAP1 and its head group-acylated products.

Understanding the changes in peanut (Arachis hypogaea L.) anther lipidome under heat stress (HT) will aid in understanding the mechanisms of heat tolerance. We profiled the anther lipidome of seven genotypes exposed to ambient temperature (AT) or HT during flowering. Under AT and HT, the lipidome was dominated by phosphatidylcholine (PC), phosphatidylethanolamine (PE), and triacylglycerol (TAG) species (> 50% of total lipids). Of 89 lipid analytes specified by total acyl carbons:total carbon-carbon double bonds, 36:6, 36:5, and 34:3 PC and 34:3 PE (all contain 18:3 fatty acid and decreased under HT) were the most important lipids that differentiated HT from AT. Heat stress caused decreases in unsaturation indices of membrane lipids, primarily due to decreases in highly-unsaturated lipid species that contained 18:3 fatty acids. In parallel, the expression of Fatty Acid Desaturase 3-2 (FAD3-2; converts 18:2 fatty acids to 18:3) decreased under HT for the heat-tolerant genotype SPT 06-07 but not for the susceptible genotype Bailey. Our results suggested that decreasing lipid unsaturation levels by lowering 18:3 fatty-acid amount through reducing FAD3 expression is likely an acclimation mechanism to heat stress in peanut. Thus, genotypes that are more efficient in doing so will be relatively more tolerant to HT.

Heat-induced changes in lipidome and their influence on stress adaptation are not well-defined in plants. We investigated if lipid metabolic changes contribute to differences in heat stress responses in a heat-tolerant soybean genotype DS25-1 and a heat-susceptible soybean genotype DT97-4290. Both genotypes were grown at optimal temperatures (OT; 30/20 °C) for 15 days. Subsequently, half of the plants were exposed to heat stress (38/28 °C) for 11 days, and the rest were kept at OT. Leaf samples were collected for lipid and RNA extractions on the 9 th and 11 th days of stress, respectively. We observed a decline in the lipid unsaturation level due to a decrease in the polyunsaturated linolenic acid (18:3) content in DS25-1. When examined under OT conditions, DS25-1 and DT97-4290 showed no significant differences in the expression pattern of the Fatty Acid Desaturase ( FAD ) 2-1A , FAD2-2B , FAD2-2C , FAD3A genes. Under heat stress conditions, substantial reductions in the expression levels of the FAD3A and FAD3B genes, which convert 18:2 lipids to 18:3, were observed in DS25-1. Our results suggest that decrease in levels of lipids containing 18:3 acyl chains under heat stress in DS25-1 is a likely consequence of reduced FAD3A and FAD3B expression, and the decrease in 18:3 contributes to DS25-1's maintenance of membrane functionality and heat tolerance.