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向顶性:稻瘟病菌中分生孢子梗结构和致病性所需的一个基因座。

Acropetal: a genetic locus required for conidiophore architecture and pathogenicity in the rice blast fungus.

作者信息

Lau G W, Hamer J E

机构信息

Department of Biological Sciences, Purdue University, West Lafayette, Indiana, 47907, USA.

出版信息

Fungal Genet Biol. 1998 Jun-Jul;24(1-2):228-39. doi: 10.1006/fgbi.1998.1053.

Abstract

Fungal spores are a primary means of dissemination and are the major sources of inoculum in pathogenic species. Sporulation in the rice blast fungus Magnaporthe grisea involves the production of three-celled conidia, borne sympodially on an aerial conidiophore. A disease cycle initiates when spores are dispersed and attach to the rice plant surface. Using insertional mutagenesis we have identified a major regulator of conidiophore morphogenesis in M. grisea. A null mutation in the acropetal (ACR1) locus causes a hypermorphic conidiation phenotype where indeterminate growth of the conidial tip cell results in the production of head-to-tail (acropetal) arrays of spores. acropetal mutants are nonpathogenic and fail to undergo infection-related morphogenesis. The ACR1 locus encodes a spore-specific transcript and acr1(-) mutants fail to turn off the expression of the hydrophobin encoding gene MPG1 in dormant spores. We propose that ACR1 is a stage-specific negative regulator of conidiation that is required to establish a sympodial pattern of spore formation. Interestingly a failure to establish the correct pattern of sporulation in M. grisea results in the production of spores that cannot progress through the disease cycle. Studies of Acropetal suggest that the diverse patterns of spore ontogeny in conidial fungi arose through alterations in major genes controlling spore-specific gene expression.

摘要

真菌孢子是传播的主要方式,也是致病物种接种体的主要来源。稻瘟病菌Magnaporthe grisea的孢子形成涉及产生三细胞分生孢子,这些分生孢子在气生分生孢子梗上呈合轴式着生。当孢子扩散并附着在水稻植株表面时,病害循环开始。利用插入诱变,我们在稻瘟病菌中鉴定出了分生孢子梗形态发生的一个主要调节因子。向顶(ACR1)位点的无效突变导致一种超形态分生孢子形成表型,其中分生孢子顶端细胞的不确定生长导致产生头对尾(向顶)排列的孢子。向顶突变体无致病性,且无法进行与感染相关的形态发生。ACR1位点编码一种孢子特异性转录本,acr1(-)突变体在休眠孢子中无法关闭疏水蛋白编码基因MPG1的表达。我们提出,ACR1是分生孢子形成的阶段特异性负调节因子,是建立合轴式孢子形成模式所必需的。有趣的是,稻瘟病菌中未能建立正确的孢子形成模式会导致产生无法完成病害循环的孢子。对向顶现象的研究表明,分生孢子真菌中不同的孢子个体发育模式是通过控制孢子特异性基因表达的主要基因的改变而产生的。

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