The key to MRSA is to separate target-based resistance from enzyme-based resistance. Ordinary penicillin-resistant staphylococci secrete penicillinase, a beta-lactamase that chops the drug; that route is defeated by penicillinase-stable drugs or by inhibitor combinations such as amoxicillin with clavulanate. MRSA does something different: the chromosomal mecA gene produces PBP2a, a modified penicillin binding protein that the beta-lactam ring cannot latch onto. Since the drug target itself is changed, no amount of beta-lactamase inhibition restores activity, ruling out the amoxicillin-clavulanate option. The mecA determinant rides on the SCCmec cassette in the chromosome, so plasmid mediation is also incorrect. The single accurate statement describes the altered PBP.
\[\boxed{\text{Due to alteration in penicillin binding proteins}}\]