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The ability of Mycobacterium tuberculosis to survive during prolonged treatment has been attributed to either transient stress responses or fixed heritable drug-resistance–producing mutations. We show that phase-variation in the M. tuberculosis glpK gene represents a third type of resistance mechanism. The ability of these glpK mutants to grow slowly and then rapidly revert.

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The ability of Mycobacterium tuberculosis to survive during prolonged treatment has been attributed to either transient stress responses or fixed heritable drug-resistance–producing mutations. We show that phase-variation in the M. tuberculosis glpK gene represents a third type of resistance mechanism. The ability of these glpK mutants to grow slowly and then rapidly revert.

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The ability of Mycobacterium tuberculosis to survive during prolonged treatment has been attributed to either transient stress responses or fixed heritable drug-resistance–producing mutations. We show that phase-variation in the M. tuberculosis glpK gene represents a third type of resistance mechanism. The ability of these glpK mutants to grow slowly and then rapidly revert.