Lipidomic insights into the response of Arabidopsis sepals to mild heat stress

Arabidopsis sepals coordinate flower opening in the morning as ambient temperature rises; however, the underlying molecular mechanisms are poorly understood. Mutation of one heat shock protein encoding gene, HSP70-16, impaired sepal heat stress responses (HSR), disrupting lipid metabolism, especially sepal cuticular lipids, leading to abnormal flower opening. To further explore, to what extent, lipids play roles in this process, in this study, we compared lipidomic changes in sepals of hsp70-16 and vdac3 (mutant of a voltage-dependent anion channel, VDAC3, an HSP70-16 interactor) grown under both normal (22 °C) and mild heat stress (27 °C, mild HS) temperatures. Under normal temperature, neither hsp70-16 nor vdac3 sepals showed significant changes in total lipids; however, vdac3 but not hsp70-16 sepals exhibited significant reductions in the ratios of all detected 11 lipid classes, except the monogalactosyldiacylglycerols (MGDGs). Under mild HS temperature, hsp70-16 but not vdac3 sepals showed dramatic reduction in total lipids. In addition, vdac3 sepals exhibited a significant accumulation of plastidic lipids, especially sulfoquinovosyldiacylglycerols (SQDGs) and phosphatidylglycerols (PGs), whereas hsp70-16 sepals had a significant accumulation of triacylglycerols (TAGs) and simultaneous dramatic reductions in SQDGs and phospholipids (PLs), such as phosphatidylcholines (PCs), phosphatidylethanolamines (PEs), and phosphatidylserines (PSs). These findings revealed that the impact of mild HS on sepal lipidome is influenced by genetic factors, and further, that HSP70-16 and VDAC3 differently affect sepal lipidomic responses to mild HS. Our studies provide a lipidomic insight into functions of HSP and VDAC proteins in the plant’s HSR, in the context of floral development.