Hydrogen sulfide (HS) has recently been recognized as an important gaseous transmitter with multiple physiological effects in various species. Previous studies have shown that HS alleviated heat-induced ganoderic acids (GAs) biosynthesis, an important quality index of . However, a comprehensive understanding of the physiological effects and molecular mechanisms of HS in remains unexplored. In this study, we found that heat treatment reduced the mitochondrial membrane potential (MMP) and mitochondrial DNA copy number (mtDNAcn) in . Increasing the intracellular HS concentration through pharmacological and genetic means increased the MMP level, mtDNAcn, oxygen consumption rate level and ATP content under heat treatment, suggesting a role for HS in mitigating heat-caused mitochondrial damage in . Further results indicated that HS activates sulfide-quinone oxidoreductase (SQR) and complex III (Com III), thereby maintaining mitochondrial homeostasis under heat stress in . Moreover, SQR also mediated the negative regulation of HS to GAs biosynthesis under heat stress. Furthermore, SQR might be persulfidated under heat stress in . Thus, our study reveals a novel physiological function and molecular mechanism of HS signalling under heat stress in with broad implications for research on the environmental response of microorganisms.

中文翻译：

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热应激下硫化氢维持线粒体稳态并通过SQR调节灵芝酸生物合成


硫化氢（HS）最近被认为是一种重要的气体递质，对多种物种具有多种生理作用。先前的研究表明，HS 减轻了热诱导的灵芝酸 (GAs) 生物合成，灵芝酸是灵芝的重要质量指标。然而，对 HS 的生理效应和分子机制的全面了解仍有待探索。在这项研究中，我们发现热处理降低了线粒体膜电位（MMP）和线粒体DNA拷贝数（mtDNAcn）。通过药理学和遗传手段增加细胞内 HS 浓度，可增加热处理下的 MMP 水平、mtDNAcn、耗氧率水平和 ATP 含量，表明 HS 在减轻热引起的线粒体损伤中发挥作用。进一步的结果表明，HS 激活硫化物醌氧化还原酶 (SQR) 和复合物 III (Com III)，从而维持热应激下的线粒体稳态。此外，SQR还介导热应激下HS对GAs生物合成的负调节。此外，SQR 在热应激下可能会过硫化。因此，我们的研究揭示了热应激下 HS 信号传导的新生理功能和分子机制，对微生物环境响应的研究具有广泛的意义。