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Cyclic di-GMP is a second messenger with a role in regulation of a range of cellular functions in diverse bacteria including the virulence of pathogens. Cellular levels of cyclic di-GMP are controlled through synthesis, catalysed by the GGDEF protein domain, and degradation by EAL or HD-GYP domains. Here we report a comprehensive study of cyclic di-GMP signalling in bacterial disease in which we examine the contribution of all proteins with GGDEF, EAL or HD-GYP domains to virulence and virulence factor production in the phytopathogen Xanthomonas campestris pathovar campestris ( Xcc). Genes with significant roles in virulence to plants included those encoding proteins whose probable function is in cyclic-di-GMP synthesis as well as others (including the HD-GYP domain regulator RpfG) implicated in cyclic di-GMP degradation. Furthermore, RpfG controlled expression of a subset of these genes. A partially overlapping set of elements controlled the production of virulence factors in vitro. Other GGDEF-EAL domain proteins had no effect on virulence factor synthesis but did influence motility. These findings indicate the existence of a regulatory network that may allow Xcc to integrate information from diverse environmental inputs to modulate virulence factor synthesis as well as of cyclic di-GMP signalling systems dedicated to other specific tasks. [ABSTRACT FROM AUTHOR]

Xanthomonas oryzae pv. oryzicola (Xoc) depends on its type III secretion system (T3SS) to translocate type III secreted effectors (T3SEs), including transcription activator-like effectors (TALEs) and non-transcription activator-like effectors (non-TALEs), into host cells. T3SEs can promote the colonization of Xoc and contribute to virulence by manipulating host cell physiology. We annotated 25 genes encoding non-TALEs in Xoc strain GX01, an isolate from Guangxi in the South China's rice growing region. Through systematic mutagenesis of non-TALEs, we found that xopN , the virulence contribution of which was previously unknown for Xoc , significantly contributes to the virulence of Xoc GX01, as does avrBs2. [ABSTRACT FROM AUTHOR]