Mitochondrial quality and quantity are essential for a cell to maintain normal cellular functions. Our previous study revealed that the transcription factor MoMsn2 plays important roles in the development and virulence of Magnaporthe oryzae. However, to date, no study has reported its underlying regulatory mechanism in phytopathogens. Here, we explored the downstream target genes of MoMsn2 using a chromatin immunoprecipitation sequencing (ChIP‐Seq) approach. In total, 332 target genes and five putative MoMsn2‐binding sites were identified. The 332 genes exhibited a diverse array of functions and the highly represented were genes involved in metabolic and catalytic processes. Based on the ChIP‐Seq data, we found that MoMsn2 plays a role in maintaining mitochondrial morphology, likely by targeting a number of mitochondria‐related genes. Further investigation revealed that MoMsn2 targets the putative 3‐methylglutaconyl‐CoA hydratase‐encoding gene (MoAUH1) to control mitochondrial morphology and mitophagy, which are critical for the infectious growth of the pathogen. Meanwhile, the deletion of MoAUH1 resulted in phenotypes similar to the ΔMomsn2 mutant in mitochondrial morphology, mitophagy and virulence. Overall, our results provide evidence for the regulatory mechanisms of MoMsn2, which targets MoAUH1 to modulate its transcript levels, thereby disturbing the mitochondrial fusion/fission balance. This ultimately affects the development and virulence of M. oryzae.

中文翻译：

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转录因子MoMsn2靶向假定的3-甲基谷氨酰-CoA水合酶编码基因MoAUH1，通过稻瘟病菌中的线粒体融合/裂变平衡控制感染性生长

线粒体的质量和数量对于细胞维持正常的细胞功能至关重要。我们以前的研究表明，转录因子MoMsn2扮演的发展和毒力的重要作用稻瘟病菌。然而，迄今为止，尚无研究报道其在植物病原体中的潜在调控机制。在这里，我们使用染色质免疫沉淀测序（ChIP-Seq）方法探索了MoMsn2的下游靶基因。总共鉴定出332个靶基因和五个推定的MoMsn2结合位点。332个基因表现出各种各样的功能，其中高度代表的是参与代谢和催化过程的基因。根据ChIP-Seq数据，我们发现MoMsn2在维持线粒体形态方面可能发挥了作用，可能是通过靶向许多线粒体相关基因。进一步调查显示，MoMsn2靶向假定的3-甲基谷氨酰-CoA水合酶编码基因（MoAUH1）以控制线粒体形态和线粒体，这对于病原体的感染性生长至关重要。同时，MoAUH1的缺失导致在线粒体形态，线粒体和毒力方面的表型类似于ΔMomsn2突变体。总体而言，我们的结果为MoMsn2的调控机制提供了证据，该机制靶向MoAUH1来调节其转录水平，从而干扰线粒体融合/裂变的平衡。这最终影响了M的发育和毒力。菌。