Anaerobic arginine metabolism of Mycobacterium tuberculosis is mediated by arginine deiminase ( arcA), but is not essential for chronic persistence in an aerogenic mouse model of infection

Abstract

In many pathogens, degradation of arginine via the arginine deiminase pathway supports anaerobic metabolism. Here we show by deletion of Rv1001 ( arcA) in Mycobacterium tuberculosis that this gene functions as an arginine deiminase. Arginine metabolism in the presence of oxygen was not affected by the mutation, indicating a separate pathway for arginine degradation under aerobic conditions. Following aerosol infection in mice, the Δ arcA mutant and wild-type strain of M. tuberculosis multiplied and persisted in infected organs in a similar fashion.