The tremendous fitness cost resulted in instability of the protamine resistance in some mutants, particularly hemC and hemA mutants, and compensatory evolution by serial passage in the absence of protamine resulted in the loss of protamine resistance. Three mutants displayed nonsense mutations in cydC, a cysteine/glutathione ABC transporter thought to be involved in maintaining cellular redox balance. A cydC mutant would therefore display reduced membrane potential as well, resulting in AMP resistance.