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Article|01 Feb 2021|OPEN
Tomato SlPUB24 enhances resistance to Xanthomonas euvesicatoria pv. perforans race T3
Xin Liu1,2, Ge Meng1,2, Mengrui Wang1,2, Zilin Qian1,2, Yaxian Zhang1,2 & Wencai Yang1,2,
1Beijing Key Laboratory of Growth and Developmental Regulation for Protected Vegetable Crops, Department of Vegetable Science, China Agricultural University, Beijing 100193, China
2Joint Laboratory for International Cooperation in Crop Molecular Breeding, Ministry of Education of the People’s Republic of China, Beijing 100193, China

Horticulture Research 8,
Article number: 30 (2021)
doi: 10.1038/hortres.2021.30
Views: 440

Received: 12 Jun 2020
Revised: 02 Dec 2020
Accepted: 03 Dec 2020
Published online: 01 Feb 2021


Solanum lycopersicum var. cerasiforme accession PI 114490 has broad-spectrum resistance to bacterial spot caused by several species of Xanthomonas. Resistance is quantitatively inherited, and a common quantitative trait locus QTL-11B on chromosome 11 has been identified previously. In this study, the SlPub24 gene was characterized in QTL-11B. SlPub24 in PI 114490 was upregulated by infection with X. euvesicatoria pv. perforans race T3, but its transcription was low in the susceptible line OH 88119 whether or not it was infected by the pathogen. The differential expression of SlPub24 between PI 114490 and OH 88119 was due to great sequence variation in the promoter region. The promoter of SlPub24 in OH 88119 had very low activity and did not respond to pathogen infection. Transgenic lines of OH 88119 overexpressing SlPub24 isolated from PI 114490 showed significantly enhanced resistance, while mutants of Slpub24 generated by CRISPR/Cas9 editing showed more susceptibility to race T3 and to other races. The mutants also showed spontaneous cell death in leaves. The expression of the salicylic acid (SA) pathway gene phenylalanine ammonia-lyase (PAL) and signaling-related genes pathogenesis-related (PR1) and nonexpresser of PR1 (NPR1) were influenced by SlPub24. The content of SA in tomato plants was consistent with the level of SlPub24 expression. Furthermore, SlPUB24 interacted with the cell wall protein SlCWP and could regulate the degradation of SlCWP. The expression levels of SlCWP and SlCWINV1, a cell wall invertase gene, showed opposite patterns during pathogen infection. The activity of SlCWINV1 was lower in mutants than in PI 114490. The results are discussed in terms of the roles of the abovementioned genes, and a potential model for SlPUB24-mediated resistance to bacterial spot is proposed.