Mycobacterium tuberculosis, the causative agent of human tuberculosis, is a successful pathogen than can persist in an individual host for decades in an asymptomatic state. Despite the fact that adaptive responses of M. tuberculosis have been extensively studied at the transcriptional level, the mechanisms underlying this persistence in the host are still poorly understood. Furthermore, the emergence of drug resistant tuberculosis makes the development of effective new treatments an urgent challenge. Understanding the ability of M. tuberculosis to switch between replicating and non-replicating states during infection and disease is central to this search for improved treatments.

The number of copies of a protein produced by a cell is generally viewed as being determined by the number of mRNA transcripts, but recent findings suggest that ‘specialised ribosomes’ can modify proteome profiles by preferential translation of particular mRNA subsets, particularly in response to stress. I recently demonstrated that M. tuberculosis differs from other bacterial pathogens in expressing a greater number of transcripts that lack a sequence for ribosomal recognition. In Escherichia coli, only a few of these transcripts have been described and they are selectively translated by specialised ribosomes.

My main research interest is to investigate the role of translation regulation in the adaptive response of M. tuberculosis and its contribution to differential susceptibility to drugs that target ribosomal activities. We are investigating the importance of selective translation of particular mRNAs subsets using cutting-edge experimental techniques combined with bioinformatics analyses.