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To probe mechanisms underlying survival under antibiotic pressure, we performed a genetic screen for\n                    <jats:named-content content-type=\"genus-species\">M. tuberculosis<\/jats:named-content>\n                    mutants with altered susceptibility to treatment using the mouse model of TB. We identified multiple genes involved in a range of functions which alter sensitivity to antibiotics. In particular, we found glycerol catabolism mutants were less susceptible to treatment and that common variation in a homopolymeric region in the\n                    <jats:italic>glpK<\/jats:italic>\n                    gene was associated with drug resistance in clinical isolates. 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