Competitive control of CsNCED1-1 by CsLOB1 and CsbZIP40 triggers susceptibility to citrus canker.

Abstract

Pustule formation is pivotal for the development of the Xanthomonas citri subsp. citri (Xcc)-induced citrus canker disease (CCD). Although our previous study demonstrated that the exogenous application of abscisic acid (ABA) facilitated pustule formation induced by Xcc, the precise mechanism remains elusive. The 9-cis-epoxycarotenoid dioxygenase (NCED) is a crucial enzyme in ABA biosynthesis. This study explored the role of citrus CsNCED1-1 in CCD resistance through overexpression and RNA interference of CsNCED1-1 in Wanjincheng orange (Citrus sinensis). Our findings indicated that CsNCED1-1 negatively modulated CCD resistance by fostering ABA accumulation, concomitant with an increase in jasmonic acid (JA) and a decrease in salicylic acid (SA). Plants overexpressing CsNCED1-1 displayed shortened leaves with smaller and denser stomata along with irregular and increased palisade cells. CsLOB1 is a known susceptibility gene for CCD, and CsbZIP40 positively influences resistance to this disease. We further confirmed that CsLOB1 promoted and CsbZIP40 suppressed the transcription of CsNCED1-1 by directly binding to the CsNCED1-1 promoter. Notably, CsbZIP40 and CsLOB1 showed a competitive relationship in the regulation of CsNCED1-1 expression, with CsbZIP40 exhibiting greater competitiveness. Overall, our findings highlight that CsNCED1-1 promotes susceptibility to citrus canker by disrupting JA- and SA-mediated defense mechanisms and triggering the proliferation and remodeling of palisade cells, thereby facilitating pathogen colonization and pustule formation. This study offers novel insights into the regulatory mechanisms underlying citrus canker resistance and the role of CsNCED1-1 in citrus.