Transcriptomic and Proteomic Profiling Reveal the Key Role of AcMYB16 in the Response of Pseudomonas syringae pv. actinidiae in Kiwifruit

Abstract

Kiwifruit bacterial canker caused by Pseudomonas syringae pv. actinidiae (Psa), is an important disease of kiwifruit (Actinidia 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 Actinidia chinensis ‘Hongyang’ but decreased in the resistant cultivar of A. chinensis var. deliciosa ‘Jinkui’ in response to Psa. 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 Psa 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 Psa of ‘Jinkui,’ including the R2R3-MYB TF subgroup 4 gene AcMYB16, which was downregulated in ‘Jinkui’ but upregulated in ‘Hongyang.’ The promoter region of AcMYB16 has a MeJA responsiveness cis-acting regulatory element (CRE). Transient expression of the AcMYB16 gene in the leaves of ‘Jinkui’ induced Psa infection. Together, these data suggest that AcMYB16 acts as a repressor to regulate the response of kiwifruit to Psa 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.

Mitigation of Emergent Bacterial Pathogens Using Pseudomonas syringae pv. actinidiae as a Case Study—From Orchard to Gene and Everything in Between

“…deliciosa Jinkui but upregulated in the susceptible cultivar A. chinensis var. chinensis Hongyang in response to Psa, putatively indicating that MYB16 acts as a negative regulatory gene in response to JA in kiwifruit infected with Psa [143]. Concordantly, a significant increase in disease development was observed in plants treated with methyl jasmonate [134,151,152], and thus, it is currently acknowledged that Actinidia spp.…”

“…deliciosa, such as Jinkui, resistant hybrids from A. chinensis var. chinensis Hort16A and of A. arguta, also pinpoint the key role of several of these TFs, including the R2R3-MYB and MYB48 families [139,140,143], in the regulation of ROS-and phytohormone-mediated signaling to finally determine plant tolerance [34,141,144,145].…”

“…deliciosa Jinkui in response to Psa. [143]. JIH, a negative marker of the JA pathway that allows plants to modulate SA-mediated responses according to their needs, was upregulated in Psainfected inoculated plants, probably as a strategy to antagonize JA-mediated defenses upon Psa infection [151].…”

“…defense responses against Psa are mainly regulated by SA, whereas elicitation of the JA and ET pathways decreases plant tolerance to the pathogen. [135,143]. Nevertheless, the commonly antagonistic SA and JA pathways seem to be concertedly activated within a short period after infection as the concentration of both hormones increases in both tolerant and susceptible genotypes in the early stages of Psa infection [135,143].…”

CsMYB Transcription Factors Participate in Jasmonic Acid Signal Transduction in Response to Cold Stress in Tea Plant (Camellia sinensis)

“…MeJA regulates multiple plant processes, including organ development, cell cycle regulation, secondary metabolite biosynthesis, and defense responses to various biotic and abiotic stresses [ 3 , 4 ]. Increasing evidence has shown that MeJA plays a positive role in inducing cold stress tolerance in horticultural crops, such as mango [ 5 ], banana [ 6 ], kiwi [ 7 ], and pitaya [ 8 ]. Cold exposure rapidly induces the expression of JA biosynthesis-related genes, among which jasmonate-ZIM-domain (JAZ) proteins are important repressors of the JA signaling pathway.…”