Amongst the pathogenic Firmicutes, Spo0A has been reported to affect toxin production in multiple species. In B. anthracis a spo0A mutation results in elevated levels of AbrB, and concomitantly lower levels of the toxin genes pagA, cya and lef that are under AbrB control [17] . Similarly, the production of the emetic toxin cereulide in B. cereus is greatly repressed in a spo0A mutant, in an AbrB-dependent manner [63] . In contrast, Spo0A directly represses the expression of the cry toxin genes in B. thuringiensis and a spo0A mutant is therefore a hyper-producer of the insecticidal crystal protein [18, 21] . In Clostridium perfringens TpeL, a member of the large clostridial toxins just like TcdA and TcdB, is directly dependent on Spo0A [64] and also the production of enterotoxin in this organism seems to be (indirectly) dependent on sporulation [65, 66] .