Han Jing, Tang Xin, Wang Lingshuai, Chen Huhui, Liu Rui, Zhao Mingwen
Key Laboratory of Agricultural Environmental Microbiology, Ministry of Agriculture and Rural Affairs, PR China; Microbiology Department, College of Life Sciences, Nanjing Agricultural University, Nanjing 210095, Jiangsu, PR China.
Microbiol Res. 2025 Apr;293:128055. doi: 10.1016/j.micres.2025.128055. Epub 2025 Jan 9.
Heat stress is a prevalent environmental stressor. Previous studies have shown that heat stress drives many cellular changes in Ganoderma lucidum. Interestingly, glycolysis is activated during heat stress, which could contribute to increased heat resistance. However, the molecular mechanisms underlying the enhanced heat resistance of G. lucidum following heat exposure are not yet fully understood. In this study, we explored the possibility that acetylation modification plays a significant role in responses to abiotic stress. After heat treatment, an enhanced interaction between the deacetylase GlSIRT1 and pyruvate kinase (PK) was observed, and the acetylation level of PK was decreased. Further studies revealed that GlSIRT1 increases PK activity through deacetylation, thereby increasing pyruvate content. Consistent with these findings, both PK activity and pyruvate content were reduced in GlSIRT1 knockdown strains, which exhibited greater sensitivity to heat stress compared to the wild-type (WT) strain. Collectively, our results reveal a novel molecular mechanism by which heat treatment increases pyruvate content.
热应激是一种普遍存在的环境应激源。先前的研究表明，热应激会促使灵芝发生许多细胞变化。有趣的是，热应激期间糖酵解被激活，这可能有助于提高耐热性。然而，热暴露后灵芝耐热性增强的分子机制尚未完全了解。在本研究中，我们探讨了乙酰化修饰在应对非生物胁迫中发挥重要作用的可能性。热处理后，观察到去乙酰化酶GlSIRT1与丙酮酸激酶（PK）之间的相互作用增强，且PK的乙酰化水平降低。进一步研究表明，GlSIRT1通过去乙酰化增加PK活性，从而增加丙酮酸含量。与这些发现一致，GlSIRT1基因敲除菌株中的PK活性和丙酮酸含量均降低，与野生型（WT）菌株相比，该菌株对热应激表现出更高的敏感性。总的来说，我们的结果揭示了一种热处理增加丙酮酸含量的新分子机制。
