## 9 Transcriptional and Post-Transcriptional Regulation of _ltrpG_ and _ltrpX_  
Expression, stability, and activity of HrpG and HrpX are dependent on numerous regulatory factors. HrpG and HrpX are negatively or positively controlled by two-component system kinases and response regulators [60; 62], ATPases [102], transcriptional regulators [53; 63; 77; 81; 84; 91; 93; 103; 104; 105], small signaling molecules [74; 101] and histone-like nucleoid-structuring (H-NS) protein [106; 107; 108] (Figure 2). However, most studies do not demonstrate direct interactions with HrpG, HrpX, or their promoters and it appears that the regulatory function on this regulon by most of these factors is probably indirect. Direct interactions between _ltrpG_/_ltrpX_ and their transcriptional regulators were reported on multiple occasions (Figure 3). [PERSON] et al. demonstrated that the sigma factor RpoE homolog RpoE1 significantly contributes to virulence and _ltrp_ gene expression in _Xcc_[104] (Figure 2). Further analyses identified that RopE1 is induced in plant-mimicking media XCM1 and controls the expression of _ltrpX in vivo_[104]. RpoE1 directly binds to the _ltrpX_ promoter and promotes _in vitro_ transcription of _ltrpX_, indicating that RpoE1 directly targets this regulator [104] (Figure 3). Interestingly, RpoE1 is neither affected transcriptionally by HrpG nor affects the expression of _ltrpG_ itself, indicating that its regulatory function is independent of HrpG [104]. The _Xcc_ fits-type transcriptional regulator Flp positively regulates virulence, exoenzyme production, growth in complex media, motility, and _ltrp_ gene expression [105] (Figure 2). _In vivo_ and _in vitro_ DNA-protein analyses combined with transcriptional data demonstrate that Flp interacts with the _ltrpX_ promoter and regulates its expression, suggesting direct regulation of _ltrpX_ transcription by Flp [105] (Figure 3). GamR, a LysR-type galactose metabolism regulator, was reported to regulate _ltrpG_ and _ltrpX_ in plant-mimicking media [77]. The regulator was found to directly bind to the _ltrpG_/_ltrpX_ intergenic region, suggesting that it is a direct regulator of the two [77] (Figure 2). However, the _gamR_ mutant did not display any significant reduction in virulence _in planta_[77]. The transcriptional repressor KdgR of _Xoo_ represses the transcription of _ltrpG_ and _ltrpX_ by directly binding to their promoter regions [103]. Accordingly, _kdgR_ mutant displays enhanced virulence and higher transcriptional expression of _ltrpG_, _ltrpX_, and _ltrp_ genes [103] (Figures 2 and 3). Upstream regulation and environmental cues that affect KdgR activity remain unknown. Post-transcriptional regulation was identified for HrpG in multiple layers. The RNA transcripts of _ltrpG_ and _ltrpD_ of _Xcci_ are controlled by the CsrA/RsmA RNA-binding protein [109] by binding to the 5' UTR, which consequently promotes translation and reduces transcript degradation [41] (Figure 3). Deletion mutants of _rsmA/csrA_ in _Xcc_, _Xoo_, and _Xcci_ are non-pathogenic, cannot colonize their host or cause HR in resistant plants and display pleiotropic phenotypes including altered colony morphology, EPS production, motility, hydrolase activity, production of DSF, glycogen accumulation, and cell aggregation [110; 111; 41]. Transcriptome analyses showed that _rsmA/csrA_ mutants of all three strains exhibit a significant reduction of transcript accumulation of _ltrp_ and T3E genes, further supporting that the _ltrpG_ is under direct control of RsmA/CsrA [110; 41; 111] (Figure 2). _E. coli_ RsmA/CsrA is controlled by antagonistic RNA RsmB/CsrB [112] that does not harbor any known structural homologs in xanthomonads. A potential antagonistic small RNA, RsmU (Figure 2), was recently identified in _Xcc_[113], but environmental cues and upstream regulators of _Xanthomonas_ RsmA/CsrA and RsmU have yet to be identified.