Vitamin B12 metabolism in Mycobacterium tuberculosis
Vitamin B12 metabolism in Mycobacterium tuberculosis
- Future MicroBiology, 8(11), p.1405-1418, 2013 .
Mycobacterium tuberculosis is included among a select group of bacteria possessing the capacity for de novobiosynthesis of vitamin B12 , the largest and most complex natural organometallic cofactor. The bacillus is also able to scavenge B 12 and related corrinoids utilizing an ATP-binding cassette-type protein that is distinct from the only known bacterial B 12 -specific transporter, BtuFCD. Consistent with the inferred requirement for itamin B12 for metabolic function, the M. tuberculosisgenome encodes two B12 riboswitches and three B 12 -dependent enzymes. Two of these enzymes have been shown to operate in methionine biosynthesis (MetH)and propionate utilization (MutAB), while the function of the putative nrdZ-encoded ribonucleotide reductase remains unknown. Taken together, these observations suggest that M. tuberculosis has the capacity to regulate core metabolic functions according to B 12 availability - whether acquired via endogenous synthesis or through uptake from the host environment - and, therefore, imply that there is a role for vitamin B12 in pathogenesis, which remains poorly understood.
Mycobacterium tuberculosis is included among a select group of bacteria possessing the capacity for de novobiosynthesis of vitamin B12 , the largest and most complex natural organometallic cofactor. The bacillus is also able to scavenge B 12 and related corrinoids utilizing an ATP-binding cassette-type protein that is distinct from the only known bacterial B 12 -specific transporter, BtuFCD. Consistent with the inferred requirement for itamin B12 for metabolic function, the M. tuberculosisgenome encodes two B12 riboswitches and three B 12 -dependent enzymes. Two of these enzymes have been shown to operate in methionine biosynthesis (MetH)and propionate utilization (MutAB), while the function of the putative nrdZ-encoded ribonucleotide reductase remains unknown. Taken together, these observations suggest that M. tuberculosis has the capacity to regulate core metabolic functions according to B 12 availability - whether acquired via endogenous synthesis or through uptake from the host environment - and, therefore, imply that there is a role for vitamin B12 in pathogenesis, which remains poorly understood.