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.
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 DeltaarcA mutant and wild-type strain of M. tuberculosis multiplied and persisted in infected organs in a similar fashion.
Sürken
Michael
M
Department of Medical Microbiology and Hospital Epidemiology, Medical School Hannover, Carl-Neuberg-Strasse 1, D-30625 Hannover, Germany.
Keller
Christine
C
Röhker
Claudia
C
Ehlers
Stefan
S
Bange
Franz-Christoph
FC
D000332:Aerobiosis; D000641:Ammonia / Q000378:metabolism; D000693:Anaerobiosis; D000818:Animals; D001120:Arginine / Q000378:metabolism*; D001426:Bacterial Proteins / Q000378:metabolism*; D015169:Colony Count, Microbial; D005260:Female; D017353:Gene Deletion; D006867:Hydrolases / Q000378:metabolism*; D008168:Lung / Q000382:microbiology; D053858:Metabolic Networks and Pathways; D051379:Mice; D008810:Mice, Inbred C57BL; D008954:Models, Biological; D009169:Mycobacterium tuberculosis / Q000201:enzymology* / Q000378:metabolism*; D014774:Virulence
D001426:Bacterial Proteins; D000641:Ammonia; D001120:Arginine; D006867:Hydrolases; C019723:arginine deiminase