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Article|01 Mar 2021|OPEN
Transcription factor WRKY22 regulates canker susceptibility in sweet orange (Citrus sinensis Osbeck) by enhancing cell enlargement and CsLOB1 expression
Qin Long1 , Meixia Du1 , Junhong Long1 , Yu Xie1 , Jingyun Zhang1 , Lanzhen Xu1 , Yongrui He1 , Qiang Li1 , Shanchun Chen1 , and Xiuping Zou,1 ,
1Citrus Research Institute, Southwest University/Chinese Academy of Agricultural Sciences, Chongqing, People’s Republic of China
*Corresponding author. E-mail: chenshanchun@cric.cn,zouxiuping@cric.cn

Horticulture Research 8,
Article number: 50 (2021)
doi: https://doi.org/10.1038/s41438-021-00486-2
Views: 829

Received: 04 Oct 2020
Revised: 30 Nov 2020
Accepted: 13 Dec 2020
Published online: 01 Mar 2021

Abstract

Pathological hypertrophy (cell enlargement) plays an important role in the development of citrus canker, but its regulators are largely unknown. Although WRKY22 is known to be involved in pathogen-triggered immunity and positively regulates resistance to bacterial pathogens in Arabidopsis, rice and pepper, the CRISPR/Cas9-mediated partial knockout of CsWRKY22 improves resistance to Xanthomonas citri subsp. citri (Xcc) in Wanjincheng orange (Citrus sinensis Osbeck). Here, we demonstrate that CsWRKY22 is a nucleus-localized transcriptional activator. CsWRKY22-overexpressing plants exhibited dwarf phenotypes that had wrinkled and thickened leaves and were more sensitive to Xcc, whereas CsWRKY22-silenced plants showed no visible phenotype changes and were more resistant to Xcc. Microscopic observations revealed that the overexpression of CsWRKY22 increased cell size in the spongy mesophyll. Transcriptome analysis showed that cell growth-related pathways, such as the auxin and brassinosteroid hormonal signaling and cell wall organization and biogenesis pathways, were significantly upregulated upon CsWRKY22 overexpression. Interestingly, CsWRKY22 activated the expression of CsLOB1, which is a key gene regulating susceptibility to citrus canker. We further confirmed that CsWRKY22 bound directly to the W-boxes just upstream of the transcription start site of CsLOB1 in vivo and in vitro. We conclude that CsWRKY22 enhances susceptibility to citrus canker by promoting host hypertrophy and CsLOB1 expression. Thus, our study provides new insights into the mechanism regulating pathological hypertrophy and the function of WRKY22 in citrus.