Biochemical and molecular studies on sporulation in bacillus anthracis

Abstract

The etiological agent of anthrax, Bacillus anthracis, is a uniquely pervasive and persistent environmental pathogen due to its ability to form dormant spores that are resistant to adverse environmental conditions such as extremes of temperature, UV radiation, and antimicrobial chemical agents. The spore is essential to the organism not only for its persistence in the environment but also for the ability of this organism to infect its hosts. Infection is initiated when spores are introduced into the host body and phagocytosed by macrophage and other phagocytic cells. It is believed that this is followed by germination of the spores into vegetative cells, with subsequent toxin gene expression and capsule production, resulting in the onset of anthrax disease. The molecular mechanism of sporulation in B. anthracis is poorly understood. The initiation of sporulation in a closely related Bacillus subtilis is controlled by the phosphorelay signal transduction system. After the genome sequence of B. anthracis was out in 2003, it was observed that the B. anthracis chromosome encodes machinery for sporulation that is broadly similar to B. subtilis. The phosphorelay of B.subtilis is activated by five histidine sensor kinases (KinA, KinB, KinC, KinD and Kin E) in response to stress signals. The target of their activation is the Spo0F response regulator (RR), to which they transfer a phosphoryl group.