The Anti-Repressor MecR2 Promotes the Proteolysis of the mecA Repressor and Enables Optimal Expression of β-lactam Resistance in MRSA
Figure 8
The mecR2 function is not dependent of mecR1 neither of the β-lactamase locus.
(A) Prototype strain HT0350 is negative for mecR1-mecI and for the β-lactamase locus. Co-overexpression of mecI and mecR2 in strain HT0350 (HT0350+mecI-mecR2), reverts the effect of mecI overexpression (HT0350+mecI). (B) The strategy used to delete mecR2 in prototype strain N315 generated an intermediate mutant that has lost the β-lactamase plasmid. The chromosomal mecR2 deletion was then transduced back to the parental strain generating a β-lactamase positive mecR2 null mutant. In both variants, the deletion of mecR2 caused a sharp decrease of the resistance level to oxacillin. (C) Prototype strain HU25 is positive for mecR2 and the β-lactamase locus and has a truncated non-functional MecI and, as such, the mecA expression is under the exclusive control of bla regulatory genes. Deletion of mecR2 in strain HU25 (HU25::ΔmecR2) has no effect on the phenotypic expression of oxacillin resistance.