In C. difficile, there are some interesting differences and similarities in the regulatory pathways. Most notably, there seems to be no phosphorelay [2] and the phosphorylation state of Spo0A is supposedly controlled by orphan histidine kinases [35] . The transcription of spo0A in C. difficile is under control of the transition state sigma factor Sigma H [37] , as it is in B. subtilis [61] . Our data indicate that both spo0A and sigH could be targets for direct regulation by Spo0A in C. difficile (Fig. 3A) , raising the possibility of auto-regulation of spo0A. The putative direct regulation of sigH by Spo0A may reflect that the C. difficile genome does not harbor a homolog of the pleiotropic regulator AbrB, which is responsible for the Spo0A-dependent regulation of sigH in B. subtilis [48] . Consistent with a model in which spo0A is positively autoregulated, we noted a sharp increase in the levels of Spo0A as cells approach the stationary growth phase ( Figure 1C) .