Discussion We previously noted that EbpR shares homology with the

AtxA/Mga family [11]. Regulators in this family this website have been shown to be active toward their target(s) in the presence of CO2 or CO2/HCO3 -. While atxA is constitutively expressed, acpA and acpB (also members of the AtxA/Mga family) as well as mga are activated by the presence of CO2. In the work described here, we present evidence that bicarbonate is a strong inducer of the ebpR-ebpABC locus and consequently of pilus presence. Among the other environmental conditions tested, pH appears to have a weak effect in the limited conditions tested, while CO2 had no effect. Although ebpR and ebpA expression levels share a similar pattern, we were not able to show that an increase in ebpR expression, beyond a certain level, resulted in a proportional further increase of ebpA expression. Finally, the Fsr system affects

expression of the ebpR-ebpABC locus independently of either the growth phase or the presence of bicarbonate. It is interesting that ebpABC, also shown to be important for E. faecalis virulence, responded to bicarbonate. Bicarbonate influences expression of adcA (encoding an adhesin I-BET-762 research buy [28]) and kfc (encoding a factor important for gut colonization) in C. rodentium, which are controlled by the bicarbonate regulator RegA [19], as well as the three toxin genes in B. anthracis [25]. Bicarbonate-mediated

transcriptional activation may be a system to sense a change in the environment. For example, the proximal portion of the duodenum is exposed to Niclosamide intermittent pulses of gastric H(+) discharged by the stomach. To protect the epithelial surface, at least two HCO3 -/Cl- anion exchangers have been described as being responsible for the C646 release of HCO3 – into the duodenum lumen [29]. We postulate that E. faecalis may be sensing this signal and consequently produces adhesin structures like the ebpABC-encoded pili to favor colonization of the intestinal track, similar to adcA in C. rodentium, the expression of which is controlled by bicarbonate and whose gene product has been shown to be involved in adherence to mammalian cells [28]. From the various results obtained in this study where expression of ebpA followed the same expression profile as the ebpR expression, we postulated that the ebpA expression level was proportionally linked to the ebpR expression. To investigate our hypothesis, we used an ebpR construct under the control of a nisin regulated promoter. However, as shown in Fig. 6, the ebpR expression level was already 2-fold higher in the complemented ΔebpR strain (in the absence of nisin) when compared to its native level in wild type OG1RF (0.06 vs. 0.03) and was not detected (with a detection level of 10-5 the level of gyrB) in the ebpR deletion mutant with the empty plasmid.