Which gene mutations confer resistance to the antibiotic isoniazid?

The mutations in the katG and inhA genes are well-documented as conferring resistance to isoniazid, a first-line antibiotic used to treat tuberculosis. The katG gene encodes for the enzyme catalase-peroxidase, which is essential for the activation of isoniazid into its active form that inhibits mycolic acid synthesis, crucial for the bacterial cell wall. Mutations in katG result in the loss of this enzymatic activity, preventing the drug from being activated, and hence allowing the bacteria to survive.

The inhA gene, on the other hand, is involved in the synthesis of mycolic acids as well, and mutations here can alter the target site for the activated isoniazid. Changes in inhA can affect the binding affinity of isoniazid, leading to resistance.

Understanding the mechanisms of these mutations is critical for both the treatment of tuberculosis and the development of new therapeutic strategies. Other gene mutations mentioned in the incorrect options relate to resistance mechanisms for different antibiotics or other roles that are not directly associated with isoniazid. For instance, rpoB mutations are linked to rifampicin resistance and mecA is associated with methicillin resistance in Staphylococcus aureus, while ABCB