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Summary: How cells drive the phospholipid signal response to heat stress (HS) to maintain cellular homeostasis is a fundamental issue in biology, but the regulatory mechanism of this fundamental process is unclear. Previous quantitative analyses of lipids showed that phosphatidylinositol (PI) accumulates after HS in Ganoderma lucidum, implying the inositol phospholipid signal may be associated with HS signal transduction. Here, we found that the PI‐4‐kinase and PI‐4‐phosphate‐5‐kinase activities are activated and that their lipid products PI‐4‐phosphate and PI‐4,5‐bisphosphate are increased under HS. Further experimental results showed that the cytosolic Ca2+ ([Ca2+]c) and ganoderic acid (GA) contents induced by HS were decreased when cells were pretreated with Li+, an inhibitor of inositol monophosphatase, and this decrease could be rescued by PI and PI‐4‐phosphate. Furthermore, inhibition of PI‐4‐kinases resulted in a decrease in the Ca2+ and GA contents under HS that could be rescued by PI‐4‐phosphate but not PI. However, the decrease in the Ca2+ and GA contents by silencing of PI‐4‐phosphate‐5‐kinase could not be rescued by PI‐4‐phosphate. Taken together, our study reveals the essential role of the step converting PI to PI‐4‐phosphate and then to PI‐4,5‐bisphosphate in [Ca2+]c signalling and GA biosynthesis under HS. [ABSTRACT FROM AUTHOR]

Ganoderma lucidum has become a potential model system for evaluating how environmental factors regulate the secondary metabolism of basidiomycetes. Heat stress (HS) is one of the most important environmental factors. It was previously reported that HS could induce the biosynthesis of ganoderic acids (GA). In this study, we found that HS increased GA biosynthesis and also significantly increased cell membrane fluidity. Furthermore, our results showed that addition of the membrane rigidifier dimethylsulfoxide (DMSO) could revert the increased GA biosynthesis elicited by HS. These results indicate that an increase in membrane fluidity is associated with HS-induced GA biosynthesis. Further evidence showed that the GA content was decreased in D9des-silenced strains and could be reverted to WT levels by addition of the membrane fluidizer benzyl alcohol (BA). In contrast, GA content was increased in D9des-overexpression strains and could be reverted to WT levels by the addition of DMSO. Furthermore, both membrane fluidity and GA biosynthesis induced by HS could be reverted by DMSO in WT and D9des-silenced strains. To the best of our knowledge, this is the first report demonstrating that membrane fluidity is involved in the regulation of heat stress induced secondary metabolism in filamentous fungi. [ABSTRACT FROM AUTHOR]