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灰葡萄孢(Botrytis cinerea)引起的灰霉病可在200多种植物上发生,每年造成全世界高达近千亿美元的损失。Atm1是一种在真核生物中进化保守的线粒体内膜ABC转运蛋白,主要通过向细胞质转运Fe/S簇参与维持细胞的正常生命活动,但Atm1在病原菌致病过程中的作用至今仍不清楚。本研究筛选到一株灰葡萄孢ATM1被T-DNA标记的致病缺陷突变体,并在野生型中对该基因实施了敲除。表型分析发现,突变体ΔBcatm1的分生孢子萌发缓慢且不同步,培养4 h的萌发率只有10%(野生型超过90%),直到12 h,萌发率才接近90%;突变体菌丝生长速度减慢,只能达到野生型水平的67%;菜豆成熟叶片离体接种实验显示,突变体ΔBcatm1基本丧失了致病能力,侵入寄主后只能在接种点附近引发微小的病斑,病斑面积只能达到野生型的10%左右。将完整的BcATM1基因重新导入突变体ΔBcatm1可以完全或部分恢复上述异常表型。本研究结果表明BcATM1是一个关键的致病相关基因,参与了灰葡萄孢分生孢子的萌发、菌丝生长及侵染寄主等过程。
Gray mold caused by Botrytis cinerea can occur on over 200 plants, causing up to nearly a hundred billion dollars a year worldwide. Atm1, an evolutionarily conserved mitochondrial ABC transporter in eukaryotes, is involved in the maintenance of normal life activities of cells by transporting Fe / S clusters to the cytoplasm. However, the role of Atm1 in pathogenic pathogenesis remains unclear . This study screened a mutant strain of ATM1 that was labeled with T-DNA in Botrytis cinerea, and knocked out the gene in wild type. Phenotypic analysis showed that the conidia germination of mutants ΔBcatm1 was slow and asynchronous, the germination rate was only 10% (wild type more than 90%) 4 h after culture, and the germination rate was close to 90% after 12 h. Growth rate slowed down, only to reach 67% of the wild-type level; Inoculated plants in vitro test showed that the mutant ΔBcatm1 basically lost the pathogenicity of invasive host can only cause tiny spots near the inoculation point, the disease The spot area can only reach about 10% of the wild type. The complete BcATM1 gene was reintroduced into the mutant ΔBcatm1 completely or partially restore the above abnormal phenotype. The results of this study indicate that BcATM1 is a key pathogenicity-related gene involved in the conidiospore germination, mycelial growth and host-infection of Botrytis cinerea.