Transcriptional Activation of Virulence Genes of Rhizobium etli.

Recently, , in addition to spp., has emerged as a prokaryotic species whose genome encodes a functional machinery for DNA transfer to plant cells. To understand this -mediated genetic transformation, it would be useful to define how its genes respond to the host plants. Here, we explored the transcriptional activation of the genes contained on the p42a plasmid. Using a reporter construct harboring under the control of the promoter, we show that the signal phenolic molecule acetosyringone (AS) induces gene expression both in an background and in an background. Furthermore, in both bacterial backgrounds, the p42a plasmid also promoted plant genetic transformation with a reporter transfer DNA (T-DNA). Importantly, the genes were transcriptionally activated by AS in a bacterial species-specific fashion in regard to the VirA/VirG signal sensor system, and this activation was induced by signals from the natural host species of this bacterium but not from nonhost plants. The early kinetics of transcriptional activation of the major genes of also revealed several features distinct from those known for : the expression of the gene reached saturation relatively quickly, and , which in is located outside the operon, was expressed only at low levels and did not respond to AS. These differences in gene transcription may contribute to the lower efficiency of T-DNA transfer of p42a than of T-DNA transfer of pTiC58 of The region encoding homologs of virulence genes in the CE3 p42a plasmid was the first endogenous virulence system encoded by the genome of a non- species demonstrated to be functional in DNA transfer and stable integration into the plant cell genome. In this study, we explored the transcriptional regulation and induction of virulence genes in and show similarities to and differences from those of their counterparts, contributing to an understanding and a comparison of these two systems. Whereas most genes in follow an induction pattern similar to that of genes, a few significant differences may at least in part explain the variations in T-DNA transfer efficiency.