Tomato SlPUB24 enhances resistance to Xanthomonas euvesicatoria pv. perforans race T3

Abstract

Solanum lycopersicumvar.cerasiformeaccession PI 114490 has broad-spectrum resistance to bacterial spot caused by several species ofXanthomonas. Resistance is quantitatively inherited, and a common quantitative trait locusQTL-11Bon chromosome 11 has been identified previously. In this study, theSlPub24gene was characterized inQTL-11B.SlPub24in PI 114490 was upregulated by infection withX.euvesicatoriapv.perforansrace T3, but its transcription was low in the susceptible line OH 88119 whether or not it was infected by the pathogen. The differential expression ofSlPub24between PI 114490 and OH 88119 was due to great sequence variation in the promoter region. The promoter ofSlPub24in OH 88119 had very low activity and did not respond to pathogen infection. Transgenic lines of OH 88119 overexpressingSlPub24isolated from PI 114490 showed significantly enhanced resistance, while mutants ofSlpub24generated 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 ofPR1 (NPR1) were influenced bySlPub24. The content of SA in tomato plants was consistent with the level ofSlPub24expression. Furthermore, SlPUB24 interacted with the cell wall protein SlCWP and could regulate the degradation of SlCWP. The expression levels ofSlCWPandSlCWINV1, 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.