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板栗疫病菌(Cryphonectria parasitica)是引起板栗疫病的一种丝状子囊菌。UV57是一个不支持病毒复制且致病力丧失的C.parasitica紫外诱变突变株。前期蛋白质组研究结果显示,蛋白86233(一种甲基转移酶)只在UV57中出现,而在野生型对照株EP155中没有检测到。为研究编码86233蛋白的cpomt基因的功能,本研究通过同源重组方法成功构建了缺失突变体Δcpomt及其互补转化株。与野生型EP155相比,Δcpomt菌株生长缓慢,色素分泌减少,产孢量降低,菌丝形态异常,对休眠板栗树枝的致病性显著降低。而在互补转化株Δcpomt-com中,这些表型及致病力变化均可以恢复到野生型水平。cpomt基因的缺失对低毒病毒CHV1-EP713的复制累积量没有影响,但导致抗逆相关基因G-α,产孢基因CLS-32,色素合成酶基因PKS转录水平明显下调。本研究为阐明甲基转移酶在病原真菌中的作用提供了新的知识。
Cryphonectria parasitica is a filamentous aspergillus that causes chestnut blight. UV57 is a UV mutagenic mutant of C. pararasitica that does not support viral replication and causes loss of virulence. Preliminary proteomics studies showed that protein 86233, a methyltransferase, appeared only in UV57, but not in wild-type control strain EP155. In order to study the function of cpomt gene encoding 86233 protein, we successfully constructed the deletion mutant Δcpomt and its complementary transformant by homologous recombination. Compared with the wild-type EP155, the strains of Acpomt grew slowly, reduced the pigment secretion, reduced the sporulation and hyphal morphology, and significantly reduced the pathogenicity of dormant chestnut branches. In the complementary transformant Δcpomt-com, these phenotypic and pathogenic changes can be restored to the wild-type level. The deletion of cpomt gene had no effect on the replication accumulation of the virulence virus CHV1-EP713, but resulted in the down-regulation of PKS transcription level of G-α, sporulation gene CLS-32 and pigment synthase gene. This study provides new insights into the role of methyltransferases in pathogenic fungi.