Characterization of HOG1 homologue, CpMK1, from Cryphonectria parasitica and evidence for hypovirus-mediated perturbation of its phosphorylation in response to hypertonic stress
Characterization of HOG1 homologue, CpMK1, from Cryphonectria parasitica and evidence for hypovirus-mediated perturbation of its phosphorylation in response to hypertonic stress
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DOI：
10.1111/j.1365-2958.2004.03919.x
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发表时间：
2004-03-01
影响因子：
3.6
通讯作者：
Kim, DH
中科院分区：
文献类型：
--
作者：
Park, SM;Choi, ES;Kim, DH
我们研究了 cpmk1 的生物学功能及其受真菌病毒的调节，cpmk1 编码 Cryphonectria parasitica 的 MAPK。序列比较显示 cpmk1 与 osm1（来自稻瘟病菌的 hog1 同源物）具有最高同源性。在高渗条件下，cpmk1 缺失突变体中观察到生长缺陷，表明 cpmk1 在功能上属于 hog1 亚家族。免疫印迹分析表明，CpMK1 通路在高渗条件下特别受到低病毒 CHV1-EP713 的影响。此外，与无病毒的同基因菌株EP155/2相比，病毒感染的低毒力UEP1菌株还表现出严重的渗透敏感性，从而为病毒调节cpmk1响应高渗应激提供了额外的证据。除了渗透敏感性之外，cpmk1 的破坏还导致一些但不是全部的低毒力相关变化，例如色素沉着、分生孢子形成、漆酶产生和泪蛋白表达减少。然而，cpmk1缺失突变体表现出信息素基因转录物积累的增加。 cpmk1 缺失突变体的毒力测定显示溃疡面积减少，但不如 UEP1 严重。这些结果表明，真菌病毒调节 MAPK，从而引发靶基因的异常表达，其中一些可能与病毒症状的发展有关。
We examined the biological function of cpmk1, which encodes a MAPK of Cryphonectria parasitica, and its regulation by mycovirus. Sequence comparisons revealed that cpmk1 had highest homology with osm1, a hog1-homologue from Magnaporthe grisea. A growth defect was observed in the cpmk1-null mutant under hyperosmotic conditions, indicating that cpmk1 functionally belongs to a hog1 subfamily. Immunoblot analyses indicated that the CpMK1 pathway was affected specifically in hyperosmotic conditions by the hypovirus CHV1-EP713. Moreover, the virus-infected hypovirulent UEP1 strain also exhibited severe osmosensitivity compared to the virus-free isogenic strain EP155/2, thus providing additional evidence for viral regulation of cpmk1 in response to a hypertonic stress. Besides osmosensitivity, disruption of cpmk1 resulted in several, but not all, hypovirulence-associated changes, such as reduced pigmentation, conidiation, laccase production and cryparin expression. However, the cpmk1-null mutant exhibited an increased accumulation of pheromone gene transcripts. Virulence assays of the cpmk1-null mutant revealed reduced canker area, but not as severe as that of UEP1. These results suggest that mycoviruses modulate the MAPK and thereby provoke the aberrant expression of target genes, some of which are likely to be implicated in viral symptom development.