浙江农业学报 ›› 2018, Vol. 30 ›› Issue (6): 999-1007.DOI: 10.3969/j.issn.1004-1524.2018.06.16

• 植物保护 • 上一篇    下一篇

GCK家族蛋白激酶MoSOK1调控稻瘟病菌的生长发育与致病性

冯晓晓1, 李海娇2, 李玲3, 4, 王教瑜3, *, 林福呈1, 卢建平2, *   

  1. 1.水稻生物学国家重点实验室,浙江大学 生物技术研究所,浙江 杭州310058;
    2.浙江大学 生命科学学院,浙江 杭州310058;
    3.浙江省农业科学院 植物保护与微生物研究所,浙江 杭州310021;
    4.浙江农林大学 农业与食品科学学院,浙江 杭州 311300
  • 收稿日期:2018-01-05 出版日期:2018-06-20 发布日期:2018-07-02
  • 通讯作者: 卢建平,E-mail: jplu@zju.edu.cn;王教瑜,E-mail: wangjiaoyu78@sina.com
  • 作者简介:冯晓晓(1982—),女,浙江玉环人,硕士,助理实验师,主要从事植物真菌病害致病机理及防控研究。E-mail: xxvon@zju.edu.cn
  • 基金资助:
    国家自然科学基金(31170136,31371891,31470249)

MoSOK1, a putative germinal center kinase encoding gene, is required for fungal growth, conidiation and pathogenicity in Magnaporthe oryzae

FENG Xiaoxiao1, LI Haijiao2, LI Ling3, 4, WANG Jiaoyu3, *, LIN Fucheng1, LU Jianping2, *   

  1. 1. State Key Laboratory of Rice Biology, Biotechnology Institute, Zhejiang University, Hangzhou 310058, China;
    2. College of Life Science, Zhejiang University, Hangzhou 310058, China;
    3. Institute of Plant Protection and Microbiology, Zhejiang Academy of Agricultural Sciences, Hangzhou 310021, China;
    4. College of Agriculture and Food Science, Zhejiang A and F University, Hangzhou 311300, China
  • Received:2018-01-05 Online:2018-06-20 Published:2018-07-02

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(MoSOK1)进行了分析。MoSOK1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,MoSOK1基因在附着胞分化关键期上调表达;与野生型菌株相比,MoSOK1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,MoSOK1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,MoSOK1基因参与稻瘟病菌生长发育和致病过程。

关键词: 稻瘟病菌, 致病相关基因, MoSOK1

Abstract: 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(MoSOK1). MoSOK1 was up-regulated during conidial germination and appressorial formation. Targeted gene replacement showed that MoSOK1 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. MoSOK1 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.

Key words: Magnaporthe oryzae, fungal pathogenicity, MoSOK1

中图分类号: