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一个 MADS-box 转录因子 MoMcm1 对于稻瘟病菌的雄性育性、小孢子产生和毒性是必需的。

A MADS-box transcription factor MoMcm1 is required for male fertility, microconidium production and virulence in Magnaporthe oryzae.

机构信息

Purdue-NWAFU Joint Research Center, Department Botany and Plant Pathology, Purdue University, West Lafayette, IN 47907, USA.

出版信息

Mol Microbiol. 2011 Apr;80(1):33-53. doi: 10.1111/j.1365-2958.2011.07556.x. Epub 2011 Feb 10.

Abstract

Appressorium formation is a key step in the infection cycle of Magnaporthe oryzae. Mst12 is a transcription factor essential for appressorium penetration and invasive growth. In this study we used the affinity purification approach to identify proteins that physically associate with Mst12. One of the Mst12-interacting genes identified was MoMCM1, which encodes a MADS-box protein orthologous to yeast Mcm1. MoMcm1 interacted with both Mst12 and Mata-1 in yeast two-hybrid assays. Deletion of MoMCM1 resulted in the loss of male fertility and microconidium production. The Momcm1 mutant was defective in appressorium penetration and formed narrower invasive hyphae, which may be responsible for its reduced virulence. In transformants expressing MoMCM1-eGFP fusion, GFP signals were observed in the nucleus. We also generated the Momcm1 mst12 double mutant, which was defective in penetration and non-pathogenic. On hydrophilic surfaces, germ tubes produced by the double mutant were severely curved, and 20% of them formed appressoria. In contrast, the Momcm1 or mst12 mutant did not form appressoria on hydrophilic surfaces. These results suggest that MoMCM1 and MST12 have overlapping functions to suppress appressorium formation under non-conducive conditions. MoMcm1 may interact with Mst12 and MatA-1 to regulate germ tube identity and male fertility respectively.

摘要

附着胞的形成是稻瘟病菌感染周期的关键步骤。Mst12 是一个转录因子,对附着胞穿透和侵袭性生长是必需的。在这项研究中,我们使用亲和纯化的方法来鉴定与 Mst12 物理结合的蛋白质。鉴定出的与 Mst12 相互作用的基因之一是 MoMCM1,它编码一个与酵母 Mcm1 同源的 MADS 框蛋白。MoMcm1 在酵母双杂交实验中与 Mst12 和 Mata-1 相互作用。MoMCM1 的缺失导致雄性不育和小分生孢子的产生丧失。Momcm1 突变体在附着胞穿透和形成更窄的侵袭性菌丝方面存在缺陷,这可能是其毒力降低的原因。在表达 MoMCM1-eGFP 融合蛋白的转化体中,观察到 GFP 信号在核内。我们还生成了 Momcm1 mst12 双突变体,它在穿透和非致病性方面存在缺陷。在亲水表面上,双突变体产生的芽管严重弯曲,其中 20%形成附着胞。相比之下,Momcm1 或 mst12 突变体在亲水表面上不会形成附着胞。这些结果表明,MoMCM1 和 MST12 在非适宜条件下具有抑制附着胞形成的重叠功能。MoMcm1 可能与 Mst12 和 MatA-1 相互作用,分别调节芽管的身份和雄性育性。

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