摘要
稻瘟病菌致病相关基因功能的研究有助于揭示其致病机理,为稻瘟病防治提供理论依据。本研究利用基因替换技术对稻瘟病菌SOK1同源基因(Mo SOK1)进行了分析。Mo SOK1编码GCK(germinal center kinase)家族的Ste20蛋白激酶,其与全蚀病菌中对应蛋白具有最高同源性。本研究表明,Mo SOK1基因在附着胞分化关键期上调表达;与野生型菌株相比,Mo SOK1基因缺失突变体菌落颜色加深,气生菌丝减少,生长速度变慢,产孢量下降,分生孢子萌发延迟,致病性降低。另外,交配实验表明,Mo SOK1基因缺失突变体能够进行交配,但产子囊壳能力降低。本研究初步表明,Mo SOK1基因参与稻瘟病菌生长发育和致病过程。
SOK1 is a Ste20 protein kinase of the germinal center kinase（ GCK） that is activated by oxidant stress and chemical anoxia. It is unknown so far whether SOK1 play roles in regulation of the fungal pathogenicity. Herein,we functionally characterized the SOK1 homologue in the rice blast fungus Magnaporthe oryzae（ Mo SOK1）. Mo SOK1 was up-regulated during conidial germination and appressorial formation. Targeted gene replacement showed that Mo SOK1 acts as a regulator to fungal development and virulence in M. oryzae. Δmosok1 mutants showed decreased vegetative growth and conidiation,delayed conidial germination and a significant reduction in virulence. Mo SOK1 was also found related to the sexual reproduction of the fungus. These data implicate that SOK1 signaling is required for fungal development and pathogenicity in phytopathogenic fungi.
作者
冯晓晓
李海娇
李玲
王教瑜
林福呈
卢建平
FENC Xiaoxiao;LI Haijiao;LI Ling;WANG Jiaoyu;LIN Fueheng;LU Jianping(State Key Laboratory of Rice Biology,Biotechnology Institute,Zhejiang University,Hangzhou 310058,China;College of Life Science,Zhejiang University,Hangzhou 310058,China;Institute of Plant Protection and Micro biology,Zhejiang Academy of Agricuhural Sciences,Hangzhou 310021,China;College of Agrieuhure and Food Science,Zhejiang A and F University,Hangzhou 311300,China)
出处
《浙江农业学报》
CSCD
北大核心
2018年第6期999-1007,共9页
Acta Agriculturae Zhejiangensis
基金
国家自然科学基金(31170136,31371891,31470249)
