Transcriptomic and Proteomic Profiling Reveal the Key Role of in the Response of pv. in Kiwifruit.

Kiwifruit bacterial canker caused by pv. (), is an important disease of kiwifruit ( Lind.). Plant hormones may induce various secondary metabolites to resist pathogens via modulation of hormone-responsive transcription factors (TFs), as reported in past studies. In this study, we showed that JA accumulated in the susceptible cultivar 'Hongyang' but decreased in the resistant cultivar of var. 'Jinkui' in response to . Integrated transcriptomic and proteomic analyses were carried out using the resistant cultivar 'Jinkui'. A total of 5,045 differentially expressed genes (DEGs) and 1,681 differentially expressed proteins (DEPs) were identified after infection. Two pathways, 'plant hormone signal transduction' and 'phenylpropanoid biosynthesis,' were activated at the protein and transcript levels. In addition, a total of 27 R2R3-MYB transcription factors (TFs) were involved in the response to of 'Jinkui,' including the R2R3-MYB TF subgroup 4 gene , which was downregulated in 'Jinkui' but upregulated in 'Hongyang.' The promoter region of has a MeJA responsiveness -acting regulatory element (CRE). Transient expression of the gene in the leaves of 'Jinkui' induced infection. Together, these data suggest that acts as a repressor to regulate the response of kiwifruit to infection. Our work will help to unravel the processes of kiwifruit resistance to pathogens and will facilitate the development of varieties with resistance against bacterial pathogens.