Mycobacterium tuberculosis complex

As MTBC diverged into different lineages, so did the expression of key and metabolic pathogenic genes, as a result of mutations introducing new TANNNT Pribnow boxes and mutations that impair the function of repressors Transcripcionales. This provides clear evidence that MTBC lineages probably reflect adaptation to different human populations. In fact, modifying gene expression could be a rapid mechanism for physiological adaptation to a new environment without the need to substantially change the genome.[3]

This can be seen reflected in the way that the different MTBC clades have their own transcriptomic signature. Even single-point mutations can completely change the transcriptional profile of a strain. An example is the N1177 strain, which carries a single mutation in the rpoB gene that confers resistance to rifampicin that modified transcription levels of multiple genes.[3]

The role of methylation is more elusive, the mutation inactivation pattern seems to confirm that methylases are not preserved throughout mtBC. Transcriptional adaptation can allow M. tuberculosis isolates to optimize their infectivity and transmission in subtly different environments provided by different human host populations.[3]

• MOTT