Abstract
The resistance of different citrus genotypes to citrus canker, caused by Xanthomonas citri subsp. citri (Xcc), is quite different. In this study, four citrus genotypes with different resistance, including resistant kumquat ‘Luofu’ (Fortunella margarita), moderately resistant Ponkan ‘18–1-10’ (Citrus reticulata), moderately susceptible sweet orange ‘Newhall’ (C. sinensis) and susceptible grapefruit ‘Duncan’ (C. paradisi) were used to elucidate the resistance mechanism. The antibacterial analysis in vitro showed low concentration of H2O2 promoted growth of Xcc, whereas high concentration inhibited growth. In addition, NADPH oxidases, also known as respiratory burst oxidase homologues (rbohs), are required for H2O2 burst during infection. Subsequently, Xcc accumulation, H2O2 production and expression of CsrbohD was measured to elucidate their roles in citrus-Xcc interaction. Through the Spearman correlation and multiple linear regression analysis, we found all three factors were significantly correlated with variety resistance, which was significantly affected by H2O2 content and expression of CsrbohD. Taken together, these data indicate a feedback regulation of CsrbohD and H2O2 in citrus. When the H2O2 content was lower than the threshold, it was not sufficient to suppress Xcc growth, and more Xcc populations suppressed H2O2 production, thus forming a vicious circle. By contrast, it can suppress Xcc growth, then CsrbohD was suppressed to reduce the oxidative damage.
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