Heat stress activates phospholipase D and triggers PIP₂ accumulation at the plasma membrane and nucleus

• Published in: The Plant journal : for cell and molecular biology 2009-10, Vol.60 (1), p.10-21
• Main Authors: Mishkind, Michael, Vermeer, Joop E.M, Darwish, Essam, Munnik, Teun
• Format: Article
• Language: English
• Subjects: Biochemistry; Biological and medical sciences; Botany; Fundamental and applied biological sciences. Psychology; heat stress; Membranes; phosphatidic acid; phosphatidylinositol 4,5-bisphosphate; phospholipid signaling; Plant physiology and development; Signal transduction; Temperature
• ISSN: 0960-7412; 1365-313X
• DOI: 10.1111/j.1365-313X.2009.03933.x

Heat stress induces an array of physiological adjustments that facilitate continued homeostasis and survival during periods of elevated temperatures. Here, we report that within minutes of a sudden temperature increase, plants deploy specific phospholipids to specific intracellular locations: phospholipase D (PLD) and a phosphatidylinositolphosphate kinase (PIPK) are activated, and phosphatidic acid (PA) and phosphatidylinositol 4,5-bisphosphate (PIP₂) rapidly accumulate, with the heat-induced PIP₂ localized to the plasma membrane, nuclear envelope, nucleolus and punctate cytoplasmic structures. Increases in the steady-state levels of PA and PIP₂ occur within several minutes of temperature increases from ambient levels of 20-25°C to 35°C and above. Similar patterns were observed in heat-stressed Arabidopsis seedlings and rice leaves. The PA that accumulates in response to temperature increases results in large part from the activation of PLD rather than the sequential action of phospholipase C and diacylglycerol kinase, the alternative pathway used to produce this lipid. Pulse-labelling analysis revealed that the PIP₂ response is due to the activation of a PIPK rather than inhibition of a lipase or a PIP₂ phosphatase. Inhibitor experiments suggest that the PIP₂ response requires signalling through a G-protein, as aluminium fluoride blocks heat-induced PIP₂ increases. These results are discussed in the context of the diverse cellular roles played by PIP₂ and PA, including regulation of ion channels and the cytoskeleton.