The two chitinases are expressed only at background levels, and it is known that nutrientpoor conditions as well as the presence of an inducer are required for their full induction. As is common with carbon utilization systems, stringent regulatory controls are in place to ensure chitinase expression only occurs under desired conditions. These include transcriptional dependence on the major global regulators sB and PrfA, as well as negative regulation by the small RNA LhrA, which we have previously shown to be negatively controlling translation of chiA, by binding to its mRNA and preventing ribosome recruitment. Numerous bacterial organisms are chitinolytic and produce chitinases that aid them in nutrient acquisition, as well as in virulence. However, chitinase production is not constant throughout bacterial growth. Rather, it occurs mostly within a narrow window of nutrient limitation under the presence of an inducer, and is considered to be subject to stringent regulatory controls. A moderate effect of the deletion was already seen on the transcript levels of chiA, but not of chiB. The observed reduction in the transcript levels of chiA is in agreement with a previous study by Riedel and colleagues, who recorded a similar effect in a microarray setting, albeit under different conditions. However, this effect was not seen in a microarray study by Garmyn and colleagues, who studied a mutant lacking agrA. This discrepancy may be a result of the conditions used for the microarray assay, which involved rich medium, 37 uC and no chitinase inducer, i.e. conditions under which chitinase transcription is normally very low. No transcriptional effect was described for chiB in either of the two microarray studies, which is in accordance with our results. Despite the lack of an effect at the transcript level, we found the extracellular levels of ChiB to also be reduced in the DagrD mutant, suggesting a post-transcriptional effect. This may be related to the altered expression of chiA in the mutant, as the deletion of chiA appears to cause a decrease in the production of ChiB. The exact nature of the post-transcriptional effect on chiB remains unknown, but mechanisms such as modulation of translation, protein stability and/or secretion could be involved. Interestingly, we also found agr itself to be induced upon chitin addition in stationary phase, in a manner similar to that seen for chiA. In S. aureus, agr-based regulation is mainly mediated through the sRNA RNAIII that acts as an effector for the system. However, in Listeria no sRNA has been identified in connection with the agr system so far. The recent recognition of the sRNA LhrA as a negative regulator of chiA prompted us to investigate whether it could be an intermediate component, mediating, at least partially, the response between agr and chiA. In support of this hypothesis, we found agrD to be a negative regulator of LhrA.