Bacillus cereus, Bacillus anthracis and Bacillus thuringiensis, are Gram-positive, spore- forming bacteria and principle members of the Bacillus cereus sensu lato complex. The species are highly similar at a chromosomal level, but are phenotypically diverse due to the presence of different plasmids. The anthrax pathogen, B. anthracis contains two virulence plasmids, pXO1 and pXO2. The pXO1 plasmid carries the anthrax toxin genes which are involved in intracellular survival and suppression of immune cell function while pXO2 carries capsule genes which are required for the pathogen to evade phagocytosis. Both plasmids are required to allow B. anthracis to act as a highly virulent mammalian pathogen. As well as encoding toxins, the pXO1 plasmid encodes atxA, a transcriptional regulator that is able to control gene expression from both the plasmid and chromosome. It is proposed that AtxA is incompatible with the chromosomally encoded PlcR, a global transcriptional regulator which controls expression of secreted haemolytic and cytolytic toxins. This has led to the genetic inactivation of plcRin all B. anthracis isolates and driven the evolution of high mammalian virulence. Interestingly, there are several B. cereus isolates that possess a pXO1-like plasmid, called pBCXO1, which are capable of inducing an anthrax like illness. Importantly, genome sequencing of one such strain, B. cereus G9241, revealed intact copies of both atxA and plcRgenes. This project aims to understand how G9241 has evolved to accommodate both regulators. We have used a pBCXO1-cured strain of G9241 to study the influence of AtxA and pBCXO1 on the biology of G9241 and how it interacts with human macrophage.

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