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植物病原菌林氏炭疽菌中一种STE12样转录因子的调控与作用

Regulation and role of a STE12-like transcription factor from the plant pathogen Colletotrichum lindemuthianum.

作者信息

Wong Sak Hoi Joanne, Herbert Corentin, Bacha Nafees, O'Connell Richard, Lafitte Claude, Borderies Gisèle, Rossignol Michel, Rougé Pierre, Dumas Bernard

机构信息

UMR 5546 CNRS-Université Paul Sabatier Toulouse III, Pôle de Biotechnologie Végétale, 24 Chemin de Borde-Rouge, BP42617 Auzeville, 31326 Castanet-Tolosan, France.

出版信息

Mol Microbiol. 2007 Apr;64(1):68-82. doi: 10.1111/j.1365-2958.2007.05639.x.

Abstract

In phytopathogenic fungi, STE12-like genes encode transcription factors essential for appressorium-mediated host penetration. However, their regulation and downstream targets are still unknown. In the present study, a STE12-like gene (CLSTE12) from Colletotrichum lindemuthianum was isolated. We identified a spliced variant whose expression was negatively regulated during early stages of pathogenesis, whereas the correctly spliced mRNA remained expressed up to the penetration step, suggesting distinct roles for these two transcripts. Indeed, the full-length sequence was able to complement a yeast STE12 mutant, whereas overexpression of the transcript variant had a dominant-negative effect on yeast invasive growth and C. lindemuthianum pathogenicity. To further investigate the downstream genes that could be regulated by CLSTE12, disruption mutants were generated. Phenotypic analyses of the mutants revealed reduced pectinase activity and conidial adhesion to polystyrene. Analysis of cell surface proteins allowed the identification of a major protein, Clsp1p, which was absent from the mutants. Clsp1p belongs to a new family of wall-associated proteins only found in euascomycetous fungi. Overall, these results suggest that the activity of CLSTE12 can be modulated by a regulated alternative splicing mechanism and that this factor is involved in the production of cell surface proteins and host cell wall degrading enzymes.

摘要

在植物病原真菌中,STE12样基因编码对附着胞介导的宿主穿透至关重要的转录因子。然而,它们的调控机制和下游靶点仍然未知。在本研究中,从菜豆炭疽菌中分离出一个STE12样基因(CLSTE12)。我们鉴定出一种剪接变体,其表达在发病早期受到负调控,而正确剪接的mRNA在穿透阶段之前一直保持表达,这表明这两种转录本具有不同的作用。事实上,全长序列能够互补酵母STE12突变体,而转录本变体的过表达对酵母侵袭性生长和菜豆炭疽菌致病性具有显性负效应。为了进一步研究可能受CLSTE12调控的下游基因,构建了缺失突变体。对突变体的表型分析显示果胶酶活性降低以及分生孢子对聚苯乙烯的粘附性降低。对细胞表面蛋白的分析鉴定出一种主要蛋白Clsp1p,该蛋白在突变体中不存在。Clsp1p属于仅在真子囊菌中发现的一个新的壁相关蛋白家族。总体而言,这些结果表明CLSTE12的活性可通过一种受调控的可变剪接机制进行调节,并且该因子参与细胞表面蛋白和宿主细胞壁降解酶的产生。

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