PrkC, a Transmembrane Serine/Threonine Protein Kinase, Regulates Bacterial Chain Length in Bacillus anthracis

Anthrax is a zoonotic disease caused by Bacillus anthracis, a spore-forming pathogen that displays a chaining phenotype. It has been reported that the chaining phenotype acts as a virulence factor in B. anthracis. In this study, we identify a serine/threonine protein kinase of B. anthracis, PrkC, the only kinase localized at the bacterium-host interface, as a determinant of B. anthracis chain length. In vitro, a prkC disruption strain (BAS Delta prkC) grew as shorter chains throughout the bacterial growth cycle. A comparative analysis between the parent strain and the BAS Delta prkC strain indicated that the levels of proteins BslO and Sap, associated with the regulation of bacterial chain length, were upregulated in the BAS Delta prkC strain. BslO is a septal murein hydrolase that catalyzes daughter cell separation, and Sap is an S-layer structural protein required for the septal localization of BslO. PrkC disruption also had a significant effect on bacterial growth, cell wall thickness, and septum formation. Upregulation of ftsZ in the BAS Delta prkC strain was also observed. Altogether, our results indicate that PrkC is required for maintaining optimum growth, cell wall homeostasis, and, most importantly, the chaining phenotype. IMPORTANCE Chaining phenotype acts as a virulence factor in Bacillus anthracis. This is the first study that identifies a signal transduction protein with an ability to regulate the chaining phenotype in Bacillus anthracis. We show that the disruption of the lone surface-localized serine/threonine protein kinase, PrkC, leads to the shortening of the bacterial chains. We report upregulation of the dechaining proteins in the PrkC disruption strain. Apart from this, we also report, for the first time, that PrkC disruption results in attenuated cell growth, a decrease in cell wall thickness, and aberrant cell septum formation during the logarithmic phase of growth, a growth phase where PrkC is expressed maximally.

Automated summary

The study identifies a serine/threonine protein kinase, PrkC, in Bacillus anthracis, which plays a role in regulating the chaining phenotype of the bacteria. PrkC disruption leads to shorter bacterial chains and upregulation of proteins associated with dechaining. This disruption also affects bacterial growth, cell wall thickness, and septum formation.