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本文引用的文献

1
The transcription factor Rbf1 is the master regulator for b-mating type controlled pathogenic development in Ustilago maydis.转录因子 Rbf1 是 Ustilago maydis 中 b-交配型控制致病性发育的主要调节因子。
PLoS Pathog. 2010 Aug 5;6(8):e1001035. doi: 10.1371/journal.ppat.1001035.
2
Regulation of pathogenic development in the corn smut fungus Ustilago maydis.调控玉米黑粉菌致病发育的机制。
Mol Plant Pathol. 2000 Jan 1;1(1):61-6. doi: 10.1046/j.1364-3703.2000.00008.x.
3
Maize tumors caused by Ustilago maydis require organ-specific genes in host and pathogen.玉米瘤由玉米黑粉菌引起,需要宿主和病原体中特定的器官基因。
Science. 2010 Apr 2;328(5974):89-92. doi: 10.1126/science.1185775.
4
Cell cycle-mediated regulation of plant infection by the rice blast fungus.细胞周期对水稻稻瘟病菌侵染植物的调控。
Plant Cell. 2010 Feb;22(2):497-507. doi: 10.1105/tpc.109.072447. Epub 2010 Feb 26.
5
The Ustilago maydis b mating type locus controls hyphal proliferation and expression of secreted virulence factors in planta.玉米黑粉菌 b 交配型位点控制菌丝增殖和在植物体内表达分泌毒力因子。
Mol Microbiol. 2010 Jan;75(1):208-20. doi: 10.1111/j.1365-2958.2009.06984.x. Epub 2009 Nov 25.
6
The germinal centre kinase Don3 triggers the dynamic rearrangement of higher-order septin structures during cytokinesis in Ustilago maydis.生发中心激酶Don3在玉米黑粉菌胞质分裂过程中触发高阶Septin结构的动态重排。
Mol Microbiol. 2009 Dec;74(6):1484-96. doi: 10.1111/j.1365-2958.2009.06948.x. Epub 2009 Nov 10.
7
A role for the DNA-damage checkpoint kinase Chk1 in the virulence program of the fungus Ustilago maydis.DNA 损伤检查点激酶 Chk1 在真菌 Ustilago maydis 毒力程序中的作用。
J Cell Sci. 2009 Nov 15;122(Pt 22):4130-40. doi: 10.1242/jcs.052233. Epub 2009 Oct 27.
8
Two NDR kinase-MOB complexes function as distinct modules during septum formation and tip extension in Neurospora crassa.两个 NDR 激酶-MOB 复合物在构巢曲霉的隔膜形成和尖端延伸过程中作为不同的模块发挥作用。
Mol Microbiol. 2009 Nov;74(3):707-23. doi: 10.1111/j.1365-2958.2009.06896.x. Epub 2009 Sep 28.
9
The dual specificity phosphatase Rok1 negatively regulates mating and pathogenicity in Ustilago maydis.双特异性磷酸酶Rok1对玉米黑粉菌的交配和致病性起负调控作用。
Mol Microbiol. 2009 Jul;73(1):73-88. doi: 10.1111/j.1365-2958.2009.06747.x. Epub 2009 May 26.
10
Hap2 regulates the pheromone response transcription factor prf1 in Ustilago maydis.Hap2 调控 Ustilago maydis 中的信息素反应转录因子 prf1。
Mol Microbiol. 2009 May;72(3):683-98. doi: 10.1111/j.1365-2958.2009.06676.x.

玉米黑粉菌 Clp1 蛋白协调信息素和 b 依赖性信号通路以协调细胞周期和致病性发育。

The Ustilago maydis Clp1 protein orchestrates pheromone and b-dependent signaling pathways to coordinate the cell cycle and pathogenic development.

机构信息

Department of Genetics, Karlsruhe Institute of Technology, 76187 Karlsruhe, Germany.

出版信息

Plant Cell. 2010 Aug;22(8):2908-22. doi: 10.1105/tpc.110.076265. Epub 2010 Aug 20.

DOI:10.1105/tpc.110.076265
PMID:20729384
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2947178/
Abstract

Regulation of the cell cycle and morphogenetic switching during pathogenic and sexual development in Ustilago maydis is orchestrated by a concerted action of the a and b mating-type loci. Activation of either mating-type locus triggers the G2 cell cycle arrest that is a prerequisite for the formation of the infectious dikaryon; this cell cycle arrest is released only after penetration of the host plant. Here, we show that bW, one of the two homeodomain transcription factors encoded by the b mating-type locus, and the zinc-finger transcription factor Rbf1, a master regulator for pathogenic development, interact with Clp1 (clampless 1), a protein required for the distribution of nuclei during cell division of the dikaryon. In addition, we identify Cib1, a previously undiscovered bZIP transcription factor required for pathogenic development, as a Clp1-interacting protein. Clp1 interaction with bW blocks b-dependent functions, such as the b-dependent G2 cell cycle arrest and dimorphic switching. The interaction of Clp1 with Rbf1 results in the repression of the a-dependent pheromone pathway, conjugation tube formation, and the a-induced G2 cell cycle arrest. The concerted interaction of Clp1 with Rbf1 and bW coordinates a- and b-dependent cell cycle control and ensures cell cycle release and progression at the onset of biotrophic development.

摘要

玉米黑粉菌中致病性和有性发育过程中的细胞周期调控和形态发生转换是由 a 和 b 交配型基因座的协同作用协调的。激活任一交配型基因座都会触发 G2 细胞周期停滞,这是形成传染性双核体的先决条件;只有在穿透宿主植物后,这种细胞周期停滞才会被释放。在这里,我们表明,b 交配型基因座编码的两个同源域转录因子之一 bW 和锌指转录因子 Rbf1(致病性发育的主要调节剂)与 Clp1(无蹼 1)相互作用,Clp1 是双核体细胞分裂过程中核分布所必需的蛋白质。此外,我们还鉴定出 Cib1,一种以前未发现的、对致病性发育至关重要的 bZIP 转录因子,为 Clp1 的互作蛋白。Clp1 与 bW 的相互作用阻止了 b 依赖性的功能,如 b 依赖性的 G2 细胞周期停滞和二态性转换。Clp1 与 Rbf1 的相互作用导致 a 依赖性的信息素途径、交配管形成和 a 诱导的 G2 细胞周期停滞受到抑制。Clp1 与 Rbf1 和 bW 的协同相互作用协调了 a 和 b 依赖性的细胞周期控制,并确保了生物营养发育开始时的细胞周期释放和进展。