Elaine Davis group project:

Gene regulation

We have discovered that M. tuberculosis RecA is expressed from two promoters, one of which is DNA-damage inducible independently of LexA, the classical regulator of DNA-damage inducible genes in other bacteria. It appears that in M. tuberculosis this LexA independent mechanism of induction is primarily responsible for the induction of DNA repair genes. Therefore, we are interested in identifying the factors controlling this novel mechanism or mechanisms of gene regulation.

A mutant in the AraC family regulator Rv1931c in strain H37Rv has been isolated and shows attenuation in a mouse model of infection. Studies in progress are aimed at identifying the genes whose expression is regulated by Rv1931c, using a combination of in vivo and in vitro approaches.

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