“…However, later on, INH-resistant clinical isolates of M. tuberculosis were frequently reported to have mutations in the ribosome-binding site (RBS) of ma6A (Kapur et al, 1996;Musser et al, 1996;Rouse et al, 1995;Telenti et al, 1997;Victor et al, 1997). This observation supported the speculation that, in M. tuberculosis, MabA could be an additional target for INH and ETH, and overexpression of MabA could mediate INH resistance by virtue of increased drug titration (Musser, 1995). Hence, we decided to characterize the mabA-encoded activity and examined, by a genetic approach, whether it can be a target for INH and ETH in M. tuberculosis.…”