Well silly we would all be dead if it wasnt bonded right
The correct answer is the last statement.
If the regulatory serine is mutated to alanine, then acetyl-CoA carboxylase will get activated spontaneously and will produce malonyl-CoA. The increased concentrations of malonyl-CoA will obstruct the oxidation of fatty acids by preventing the entry of fatty acids into the mitochondria.
It is because the AMP-activated protein kinase phosphorylates the serine residues of acetyl-CoA carboxylase to inactivate it. If a mutation occurs in such residues, then the AMPL cannot phosphorylate acetyl-CoA carboxylase and this enzyme will get activated spontaneously.
In such a situation, there will be more than sufficient production of malonyl-CoA, which will inhibit the admittance of more fatty acid getting inside the mitochondria; this will indirectly prevent the oxidation of fatty acids.
