Tomato SlWRKY3 Negatively Regulates Botrytis cinerea Resistance via TPK1b

Author:

Luo Dan1ORCID,Cai Jun2,Sun Wenhui2,Yang Qihong3,Hu Guoyu2ORCID,Wang Taotao2

Affiliation:

1. College of Horticulture, Shanxi Agricultural University, Jinzhong 030801, China

2. National Key Laboratory for Germplasm Innovation and Utilization of Horticultural Crops, Huazhong Agriculture University, Wuhan 430070, China

3. Guangxi Academy of Agricultural Science, Nanning 530007, China

Abstract

Botrytis cinerea is considered the second most important fungal plant pathogen, and can cause serious disease, especially on tomato. The TPK1b gene encodes a receptor-like kinase that can positively regulate plant resistance to B. cinerea. Here, we identified a tomato WRKY transcription factor SlWRKY3 that binds to the W-box on the TPK1b promoter. It can negatively regulate TPK1b transcription, then regulate downstream signaling pathways, and ultimately negatively regulate tomato resistance to B. cinerea. SlWRKY3 interference can enhance resistance to B. cinerea, and SlWRKY3 overexpression leads to susceptibility to B. cinerea. Additionally, we found that B. cinerea can significantly, and rapidly, induce the upregulation of SlWRKY3 expression. In SlWRKY3 transgenic plants, the TPK1b expression level was negatively correlated with SlWRKY3 expression. Compared with the control, the expression of the SA pathway marker gene PR1 was downregulated in W3-OE plants and upregulated in W3-Ri plants when inoculated with B. cinerea for 48 h. Moreover, SlWRKY3 positively regulated ROS production. Overall, SlWRKY3 can inhibit TPK1b transcription in tomato, and negatively regulate resistance to B. cinerea by modulating the downstream SA and ROS pathways.

Funder

National Natural Science Foundation of China

Science and Technology Planning Project of Guangxi

Basic Research Program of Shanxi Province

Shanxi Agricultural University Doctoral Research Startup Project

Shanxi Province Excellent Doctoral Work Award-Scientific Research Project

Publisher

MDPI AG

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