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中国农学通报 ›› 2012, Vol. 28 ›› Issue (27): 163-166.

• 生物技术科学 • 上一篇    下一篇

木霉重寄生过程分子机制的研究进展

杨萍 杨谦   

  • 收稿日期:2012-02-17 修回日期:2012-03-29 出版日期:2012-09-25 发布日期:2012-09-25
  • 基金资助:

    优质水稻防病关键技术研究;哈茨木霉和毛壳菌转化子生物农药

Research Progress on Molecular Mechanism of Trichoderma Mycoparasitism

  • Received:2012-02-17 Revised:2012-03-29 Online:2012-09-25 Published:2012-09-25

摘要:

木霉(Trichoderma spp.)是一种广谱性拮抗菌,能够拮抗多种病原真菌,重寄生作用是木霉生物防治的主要机制,掌握其分子机制有利于对木霉进行合理应用和改造。为此,本研究综述了木霉重寄生过程的分子机制研究进展,包括木霉重寄生过程的信号转导途径和产生水解病原菌细胞壁的水解酶的研究概况。木霉重寄生过程中的信号转导途径主要是异源三聚体G蛋白信号和MAPK基序,分泌的细胞壁水解酶主要有几丁质酶,葡聚糖酶和蛋白酶。

关键词: 耗水量, 耗水量

Abstract:

Trichoderma spp.was a broad spectrum antagonistic fungus which could antagonized a variety of pathogenic fungi, mycoparasitism was main mechanism of Trichoderma biological control. To master the molecular mechanisms was in favor of reasonable application and transformation of Trichoderma, therefore, this article reviewed the molecular mechanism research progress of Trichoderma mycoparasitism, including the signal transduction of Trichoderma mycoparasitism and the hydrolytic enzymes producing in the process of mycoparasitism which hydrolysis of pathogenic fungi cell wall. Trichoderma signal transduction pathways in the process of mycoparasitism was heterotrimeric G-proteins and mitogen-activated protein kinase (MAPK) cascades, the cell wall-degrading enzymes of Trichoderma included chitinase, glucanase and protease.