The root-knot nematode effector Mi2G02 hijacks a host plant trihelix transcription factor to promote nematode parasitism

文献类型： 外文期刊

第一作者： Zhao, Jianlong

作者： Zhao, Jianlong;Huang, Kaiwei;Liu, Rui;Lai, Yuqing;Ling, Jian;Li, Yan;Yang, Yuhong;Xie, Bingyan;Mao, Zhenchuan;Abad, Pierre;Favery, Bruno;Quentin, Michael;Jian, Heng;Jian, Heng

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关键词： Meloidogyne incognita; effector; giant cell; transcription factor; interaction

期刊名称：PLANT COMMUNICATIONS （ 影响因子：10.5； 五年影响因子：10.5 ）

ISSN： 2590-3462

年卷期： 2024 年 5 卷 2 期

页码：

收录情况： SCI

摘要： Root-knot nematodes (RKNs) cause huge agricultural losses every year. They secrete a repertoire of effectors to facilitate parasitism through the induction of plant-derived giant feeding cells, which serve as their sole source of nutrients. However, the mode of action of these effectors and their targeted host proteins remain largely unknown. In this study, we investigated the role of the effector Mi2G02 in Meloidogyne incognita parasitism. Host-derived Mi2G02 RNA interference in Arabidopsis thaliana affected giant cell development, whereas ectopic expression of Mi2G02 promoted root growth and increased plant susceptibility to M. incognita. We used various combinations of approaches to study the specific interactions between Mi2G02 and A. thaliana GT-3a, a trihelix transcription factor. GT-3a knockout in A. thaliana affected feeding-site development, resulting in production of fewer egg masses, whereas GT-3a overexpression in A. thaliana increased susceptibility to M. incognita and also root growth. Moreover, we demonstrated that Mi2G02 plays a role in maintaining GT-3a protein stabilization by inhibiting the 26S proteasomedependent pathway, leading to suppression of TOZ and RAD23C expression and thus promoting nematode parasitism. This work enhances our understanding of how a pathogen effector manipulates the role and regulation of a transcription factor by interfering with a proteolysis pathway to reprogram gene expression for development of nematode feeding cells.

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