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灰葡萄孢中bcbrn1和bcpks13的缺失不仅会阻止黑色素形成,还会增加营养生长和毒力。

Loss of bcbrn1 and bcpks13 in Botrytis cinerea Not Only Blocks Melanization But Also Increases Vegetative Growth and Virulence.

作者信息

Zhang Chenghua, He Yifan, Zhu Pinkuan, Chen Lu, Wang Yiwen, Ni Bing, Xu Ling

机构信息

School of Life Science, East China Normal University, Shanghai 200241, PR China.

出版信息

Mol Plant Microbe Interact. 2015 Oct;28(10):1091-101. doi: 10.1094/MPMI-04-15-0085-R. Epub 2015 Sep 15.

DOI:10.1094/MPMI-04-15-0085-R
PMID:26035129
Abstract

Botrytis cinerea is a necrotrophic pathogen that causes gray mold disease in a broad range of plants. Dihydroxynaphthalene (DHN) melanin is a major component of the extracellular matrix of B. cinerea, but knowledge of the exact role of melanin biosynthesis in this pathogen is unclear. In this study, we characterize two genes in B. cinerea, bcpks13 and bcbrn1, encoding polyketide synthase and tetrahydroxynaphthalene (THN) reductases, respectively, and both have predicted roles in DHN melanin biosynthesis. The ∆bcpks13 and ∆bcbrn1 mutants show white and orange pigmentation, respectively, and the mutants are also deficient in conidiation in vitro but show enhanced growth rates and virulence on hosts. Moreover, the mutants display elevated acidification of the complete medium (CM), probably due to oxalic acid secretion and secretion of cell wall-degrading enzymes, and preferably utilize plant cell-wall components as carbon sources for mycelium growth in vitro. In contrast, overexpression of bcbrn1 (OE::bcbrn1 strain) results in attenuated hydrolytic enzyme secretion, acidification ability, and virulence. Taken together, these results indicate that bcpks13 and bcbrn1 participate in diverse cellular and developmental processes, such as melanization and conidiation in B. cinerea in vitro, but they negatively regulate the virulence of this pathogen.

摘要

灰葡萄孢是一种坏死营养型病原菌,可在多种植物上引起灰霉病。二羟基萘(DHN)黑色素是灰葡萄孢细胞外基质的主要成分,但黑色素生物合成在该病原菌中的确切作用尚不清楚。在本研究中,我们鉴定了灰葡萄孢中的两个基因,bcpks13和bcbrn1,它们分别编码聚酮合酶和四羟基萘(THN)还原酶,并且在DHN黑色素生物合成中均具有预测作用。∆bcpks13和∆bcbrn1突变体分别表现出白色和橙色色素沉着,并且这些突变体在体外也缺乏分生孢子形成,但在宿主上显示出提高的生长速率和毒力。此外,这些突变体表现出完全培养基(CM)酸化增强,这可能是由于草酸分泌和细胞壁降解酶的分泌,并且在体外优先利用植物细胞壁成分作为菌丝体生长的碳源。相反,bcbrn1的过表达(OE::bcbrn1菌株)导致水解酶分泌、酸化能力和毒力减弱。综上所述,这些结果表明bcpks13和bcbrn1参与了多种细胞和发育过程,例如灰葡萄孢在体外的黑色素化和分生孢子形成,但它们对该病原菌的毒力具有负调控作用。

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