State Key Laboratory for Managing Biotic and Chemical Threats to the Quality and Safety of Agro-products, Institute of Biotechnology, Zhejiang University, Hangzhou, China.
Ministry of Agriculture Key Laboratory of Molecular Biology of Crop Pathogens and Insects, Institute of Biotechnology, Zhejiang University, Hangzhou, China.
Microbiol Spectr. 2023 Jun 15;11(3):e0017123. doi: 10.1128/spectrum.00171-23. Epub 2023 May 16.
Autophagy is a conserved degradation and recycling pathway in eukaryotes and is important for their normal growth and development. An appropriate status of autophagy is crucial for organisms which is tightly regulated both temporally and continuously. Transcriptional regulation of () is an important layer in autophagy regulation. However, the transcriptional regulators and their mechanisms are still unclear, especially in fungal pathogens. Here, we identified Sin3, a component of the histone deacetylase complex, as a transcriptional repressor of and negative regulator of autophagy induction in the rice fungal pathogen Magnaporthe oryzae. A loss of resulted in upregulated expression of and promoted autophagy with an increased number of autophagosomes under normal growth conditions. Furthermore, we found that Sin3 negatively regulated the transcription of , , and through direct occupancy and changed levels of histone acetylation. Under nutrient-deficient conditions, the transcription of was downregulated, and the reduced occupancy of Sin3 from those resulted in histone hyperacetylation and activated their transcription and in turn promoted autophagy. Thus, our study uncovers a new mechanism of Sin3 in modulating autophagy through transcriptional regulation. Autophagy is an evolutionarily conserved metabolic process and is required for the growth and pathogenicity of phytopathogenic fungi. The transcriptional regulators and precise mechanisms of regulating autophagy, as well as whether the induction or repression of is associated with autophagy level, are still poorly understood in M. oryzae. In this study, we revealed that Sin3 acts as a transcriptional repressor of to negatively regulate autophagy level in M. oryzae. Under the nutrient-rich conditions, Sin3 inhibits autophagy with a basal level through directly repressing the transcription of . Upon nutrient-deficient treatment, the transcriptional level of would decrease and dissociation of Sin3 from those s associates with histone hyperacetylation and activates their transcriptional expression and in turn contributes to autophagy induction. Our findings are important as we uncover a new mechanism of Sin3 for the first time to negatively modulate autophagy at the transcriptional level in M. oryzae.
自噬是真核生物中一种保守的降解和回收途径,对其正常生长和发育至关重要。自噬的适当状态对于生物体是至关重要的,它受到严格的时间和连续的调节。()的转录调控是自噬调控的一个重要层次。然而,转录调节剂及其机制尚不清楚,特别是在真菌病原体中。在这里,我们鉴定出 Sin3,一种组蛋白去乙酰化酶复合物的组成部分,是水稻真菌病原体稻瘟病菌中()的转录抑制因子和自噬诱导的负调节剂。()的缺失导致其表达上调,并在正常生长条件下促进自噬,自噬体数量增加。此外,我们发现 Sin3 通过直接占据和改变组蛋白乙酰化水平来负调控()、()和()的转录。在营养缺乏的条件下,()的转录下调,从这些()中减少 Sin3 的占据导致组蛋白超乙酰化并激活其转录,并进而促进自噬。因此,我们的研究揭示了 Sin3 通过转录调控调节自噬的一种新机制。自噬是一种进化上保守的代谢过程,是植物病原真菌生长和致病性所必需的。在稻瘟病菌中,自噬的转录调节剂和精确机制,以及()的诱导或抑制是否与自噬水平相关,仍然知之甚少。在本研究中,我们揭示了 Sin3 作为()的转录抑制因子,负调控稻瘟病菌自噬水平。在营养丰富的条件下,Sin3 通过直接抑制()的转录来抑制自噬,保持基础水平。在营养缺乏处理下,()的转录水平会下降,Sin3 从这些()上解离与组蛋白超乙酰化相关,并激活其转录表达,进而促进自噬诱导。我们的发现很重要,因为我们首次揭示了 Sin3 在稻瘟病菌中通过转录水平负调控自噬的新机制。