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促分裂原活化蛋白激酶激酶 BOS5 参与调控灰葡萄孢菌的营养分化和毒性。

The mitogen-activated protein kinase kinase BOS5 is involved in regulating vegetative differentiation and virulence in Botrytis cinerea.

机构信息

Institute of Biotechnology, Zhejiang University, Hangzhou, China.

出版信息

Fungal Genet Biol. 2010 Sep;47(9):753-60. doi: 10.1016/j.fgb.2010.06.002. Epub 2010 Jun 8.

DOI:10.1016/j.fgb.2010.06.002
PMID:20595070
Abstract

We present a characterization of bos5 from Botrytis cinerea, a gene that encodes a mitogen-activated protein kinase kinase (MAPKK), which is homologous to OS-5 of Neurospora crassa. The bos5 gene deletion mutant exhibited reduced vegetative growth and strongly impaired conidiation. The mutant also exhibited increased sensitivity to the dicarboximide fungicide iprodione and to osmotic stress mediated by NaCl or KCl. Western-blot analysis showed that the BcSAK1 protein, the putative downstream component of BOS5, was not phosphorylated in the mutant. Plant inoculation tests showed that the mutants were unable to infect cucumber leaves. All of these defects were restored by genetic complementation of the Deltabcos5-21 mutant with the wild-type bos5 gene. These results indicated that BOS5 is involved in the regulation of vegetative differentiation, virulence, adaptation to iprodione and ionic stress in B. cinerea.

摘要

我们对来自 Botrytis cinerea 的 bos5 基因进行了特征描述,该基因编码一种丝裂原活化蛋白激酶激酶(MAPKK),与 Neurospora crassa 的 OS-5 同源。bos5 基因缺失突变体表现出生长势减弱和产孢能力严重受损。该突变体对二羧酰亚胺类杀菌剂异菌脲和 NaCl 或 KCl 介导的渗透胁迫也更为敏感。Western-blot 分析表明,BcSAK1 蛋白,即 BOS5 的假定下游成分,在突变体中未被磷酸化。植物接种试验表明,突变体无法感染黄瓜叶片。Deltabcos5-21 突变体与野生型 bos5 基因的遗传互补完全恢复了这些缺陷。这些结果表明 BOS5 参与调控 Botrytis cinerea 的营养分化、毒性、对异菌脲和离子胁迫的适应。

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