Identification and Functional Analysis of AopN, an <i>Acidovorax Citrulli</i> Effector that Induces Programmed Cell Death in Plants

• Main Authors: Xiaoxiao Zhang, Mei Zhao, Jie Jiang, Linlin Yang, Yuwen Yang, Shanshan Yang, Ron Walcott, Dewen Qiu, Tingchang Zhao
• Format: Article
• Language: English
• Published: MDPI AG 2020-08-01
• Series: International Journal of Molecular Sciences
• Subjects: AopN; programmed cell death; <i>Acidovorax citrulli</i>; plant pathogen; effector-triggered immunity
• Online Access: https://www.mdpi.com/1422-0067/21/17/6050
• ISSN: 1661-6596; 1422-0067

Bacterial fruit blotch (BFB), caused by <i>Acidovorax citrulli</i>, seriously affects watermelon and other cucurbit crops, resulting in significant economic losses. However, the pathogenicity mechanism of <i>A. citrulli</i> is not well understood. Plant pathogenic bacteria often suppress the plant immune response by secreting effector proteins. Thus, identifying <i>A. citrulli</i> effector proteins and determining their functions may improve our understanding of the underlying pathogenetic mechanisms. In this study, a novel effector, AopN, which is localized on the cell membrane of <i>Nicotiana benthamiana,</i> was identified. The functional analysis revealed that AopN significantly inhibited the flg22-induced reactive oxygen species burst. AopN induced a programmed cell death (PCD) response. Unlike its homologous protein, the ability of AopN to induce PCD was dependent on two motifs of unknown functions (including DUP4129 and Cpta_toxin), but was not dependent on LXXLL domain. More importantly, the virulence of the <i>aopN</i> mutant of <i>A. citrulli</i> in <i>N. benthamiana</i> significantly decreased, indicating that it was a core effector. Further analysis revealed that AopN interacted with watermelon ClHIPP and ClLTP, which responds to <i>A. citrulli</i> strain Aac5 infection at the transcription level. Collectively, these findings indicate that AopN suppresses plant immunity and activates the effector-triggered immunity pathway.