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板栗疫病菌cpomt基因的功能

发布时间:2018-07-14 19:58
【摘要】: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。
[Abstract]:Cryphonectria parasitica is a filamentous ascomycetes causing chestnut blight. UV57 is a C.parasitica UV mutant that does not support virus replication and loses pathogenicity. Previous proteome studies showed that protein 86233 (a methyltransferase) was only found in UV57, but not in wild type control strain EP155. In order to study the function of cpomt gene encoding 86233 protein, the deletion mutant 螖 cpomt and its complementary transformation strain were successfully constructed by homologous recombination method. Compared with wild type EP155, 螖 cpomt strain grew slowly, pigment secretion decreased, sporulation decreased, hyphal morphology was abnormal, pathogenicity of dormant chestnut branches was significantly decreased. In the complementary transformation strain 螖 cpomt-com, these phenotypic and pathogenicity changes could recover to the wild-type level. The deletion of cpomt gene had no effect on the replication accumulation of CHV1-EP713. However, the transcription level of G- 伪, CLS-32 and PKS was down-regulated. This study provides a new understanding of the role of methyltransferase in pathogenic fungi.
【作者单位】: 广西大学生命科学与技术学院;广西大学亚热带农业生物资源保护与利用国家重点实验室;
【基金】:国家自然科学基金(31260027) 广西自然科学基金(2014GXNSFBA118064)共同资助
【分类号】:S436.64


本文编号:2122783

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