We found that the in vitro transcription start sites of the novel SdrP-regulated genes were 6–7 bp downstream from the predicted −10 hexamers of their promoters and around 40 bp downstream of the putative SdrP-binding sites, as in the cases of the previously identified SdrP-regulated genes (Fig. 2a and Fig. S2) (Agari et al., 2008). We investigated the sequence conservation of the putative binding-sequences of 16 SdrP-regulated promoters including

those identified in the previous study (Agari et al., 2008) (Fig. 2a and b). The results indicate that the left arm of the putative binding-sites is relatively conserved as TTGTG, but the right arm is not except for two C bases (Fig. 2b). Table 2 summarizes the eight genes that are under the

control of the SdrP-dependent promoter found in this study. The gene products include manganese superoxide dismutase (TTHA0557) (Ludwig et al., 1991; Peterson et al., 1991) and catalase (TTHA1625) (Rehse et al., 2004), www.selleckchem.com/products/Dasatinib.html which are involved in the oxidative stress response, and excinuclease ABC subunit B (UvrB) (TTHA1892) (Nakagawa et al., 1999), which plays a central role in the nucleotide excision repair of damaged DNA. According to blast searches, the functions of the other gene products were predicted to be in redox control (TTHA1215, TTHA1635, and TTHB132), protein degradation (TTHA1128), and transcriptional regulation (TTHA0029). Expression of the genes also tended to increase upon entry into the stationary phase, as in the case of the

previously identified Selleck Talazoparib SdrP-regulated genes (Table 1). We could not find the predicted SdrP-binding sequence close to the promoter regions of the 16 genes whose expression showed strong negative correlation with that of the sdrP gene, suggesting that SdrP does not act Mirabegron as a transcription repressor. Thus, including the 14 previously identified genes, a total of 22 genes have been identified as SdrP-regulated genes. We analyzed the altered expression profiles of the 22 SdrP-regulated genes in cells perturbed by the various stresses, and found that the expression of most genes increased with these perturbations (Table 1). The altered expression profile caused by 2 mM diamide treatment was the most similar to that upon entry into the stationary growth phase (Table 1). The expression level did not always correlate with that of the sdrP gene, especially in response to perturbation by 50 mM tetracycline, in which the expression of 13 genes was significantly decreased (Table 1). These results suggest that depending on the stress, not only the signal via SdrP, but also other signal(s) are transmitted to the cells to alter expression of the SdrP-regulated genes. Using expression pattern analysis of a large amount of DNA microarray data, we found eight new SdrP-regulated genes that were not identified in previously studies using comparative expression analysis of the wild-type and ΔsdrP strains (Agari et al., 2008).