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Article|01 May 2020|OPEN
Citron C-05 inhibits both the penetration and colonization of Xanthomonas citri subsp. citri to achieve resistance to citrus canker disease
Hongyan Fu1,2, Mingming Zhao1,2, Jing Xu1,2, Limei Tan2, Jian Han3, Dazhi Li1,2, Meijun Wang1, Shunyuan Xiao4, Xianfeng Ma1,2, & Ziniu Deng1,2,
1College of Horticulture, Hunan Agricultural University, 410128 Changsha, Hunan, China
2National Center for Citrus Improvement, 410128 Changsha, Hunan, China
3Hunan Horticultural Research Institute, 410125 Changsha, Hunan, China
4Institute for Bioscience and Biotechnology Research & Department of Plant Sciences and Landscape Architecture, University of Maryland College Park, Rockville, MD 20850, USA

Horticulture Research 7,
Article number: 58 (2020)
doi: 10.1038/hortres.2020.58
Views: 501

Received: 07 Sep 2019
Revised: 05 Feb 2020
Accepted: 12 Feb 2020
Published online: 01 May 2020


Citrus canker, caused by Xanthomonas citri subsp. citri (Xcc), is a serious bacterial disease that affects citrus production worldwide. Citron C-05 (Citrus medica) is the only germplasm in the Citrus genus that has been identified to exhibit strong resistance to Xcc. However, it has not been determined when, where, and how Xcc is restricted in the tissues of Citron C-05 during the infection process. In the present study, we investigated the spatiotemporal growth dynamics of an eGFP-labeled virulent Xcc (eGFP-Xcc) strain in Citron C-05 along with five susceptible biotypes (i.e., lemon, pummelo, sour orange, sweet orange, and ponkan mandarin) upon inoculation via the spraying or leaf infiltration of a bacterial suspension. The results from extensive confocal laser scanning microscopy analyses showed that while Xcc grew rapidly in plants of all five susceptible genotypes, Xcc was severely restricted in the epidermal and mesophyll cell layers of the leaves of Citron C-05 in the early stage of infection. Not surprisingly, resistance against Xcc in Citron C-05 was found to be associated with the production of reactive oxygen species and hypersensitive response-like cell death, as well as greater upregulation of several defense-related genes, including a pathogenesis-related gene (PR1) and a glutathione S-transferase gene (GST1), compared with sweet orange as a susceptible control. Taken together, our results not only provide further valuable details of the spatiotemporal dynamics of the host entry, propagation, and spread of Xcc in both resistant and susceptible citrus plants but also suggest that resistance to Xcc in Citron C-05 may be attributed to the activation of multiple defense mechanisms.