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一个组蛋白去乙酰化酶,MoHOS2,调节稻瘟病菌的无性发育和毒性。

A histone deacetylase, MoHOS2 regulates asexual development and virulence in the rice blast fungus.

机构信息

Department of Biotechnology, College of Life and Applied Sciences, Yeungnam University, Gyeongsan, 38541, Republic of Korea.

出版信息

J Microbiol. 2019 Dec;57(12):1115-1125. doi: 10.1007/s12275-019-9363-5. Epub 2019 Nov 22.

DOI:10.1007/s12275-019-9363-5
PMID:31758396
Abstract

Histone acetylation/deacetylation represent a general and efficient epigenetic mechanism through which fungal cells control gene expression. Here we report developmental requirement of MoHOS2-mediated histone deacetylation (HDAC) for the rice blast fungus, Magnaporthe oryzae. Structural similarity and nuclear localization indicated that MoHOS2 is an ortholog of Saccharomyces cerevisiae Hos2, which is a member of class I histone deacetylases and subunit of Set3 complex. Deletion of MoHOS2 led to 25% reduction in HDAC activity, compared to the wild-type, confirming that it is a bona-fide HDAC. Lack of MoHOS2 caused decrease in radial growth and impinged dramatically on asexual sporulation. Such reduction in HDAC activity and phenotypic defects of ΔMohos2 were recapitulated by a single amino acid change in conserved motif that is known to be important for HDAC activity. Expression analysis revealed up-regulation of MoHOS2 and concomitant down-regulation of some of the key genes involved in asexual reproduction under sporulation-promoting condition. In addition, the deletion mutant exhibited defect in appressorium formation from both germ tube tip and hyphae. As a result, ΔMohos2 was not able to cause disease symptoms. Wound-inoculation showed that the mutant is compromised in its ability to grow inside host plants as well. We found that some of ROS detoxifying genes and known effector genes are de-regulated in the mutant. Taken together, our data suggest that MoHOS2-dependent histone deacetylation is pivotal for proper timing and induction of transcription of the genes that coordinate developmental changes and host infection in M. oryzae.

摘要

组蛋白乙酰化/去乙酰化代表了一种普遍而有效的表观遗传机制,真菌细胞通过这种机制来控制基因表达。在这里,我们报告了 MoHOS2 介导的组蛋白去乙酰化 (HDAC) 在稻瘟病菌 Magnaporthe oryzae 中的发育需求。结构相似性和核定位表明,MoHOS2 是酿酒酵母 Hos2 的同源物,后者是 I 类组蛋白去乙酰化酶和 Set3 复合物的亚基。与野生型相比,MoHOS2 的缺失导致 HDAC 活性降低了 25%,证实它是一种真正的 HDAC。MoHOS2 的缺失导致径向生长减少,并严重影响无性孢子形成。在保守基序中的一个单一氨基酸变化导致了这种 HDAC 活性的降低和ΔMohos2 的表型缺陷,该保守基序已知对 HDAC 活性很重要。表达分析显示,在促进孢子形成的条件下,MoHOS2 的表达上调,同时与无性繁殖相关的一些关键基因下调。此外,缺失突变体在从芽管尖端和菌丝形成附着胞方面表现出缺陷。因此,ΔMohos2 不能引起疾病症状。伤口接种表明,该突变体在其在宿主植物内部生长的能力上也受到了损害。我们发现,一些 ROS 解毒基因和已知的效应基因在突变体中失调。总之,我们的数据表明,MoHOS2 依赖性组蛋白去乙酰化对于协调发育变化和宿主感染的基因的适时和诱导转录至关重要。

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