Dissection of Events in
the Resistance to β-Lactam Antibiotics Mediated by the Protein
BlaR1 from <i>Staphylococcus aureus</i>
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Abstract
A heterologous expression system was used to evaluate
activation of BlaR1, a sensor/signal transducer protein of <i>Staphylococcus aureus</i> with a central role in resistance
to β-lactam antibiotics. In the absence of other <i>S.
aureus</i> proteins that might respond to antibiotics and participate
in signal transduction events, we documented that BlaR1 fragmentation
is autolytic, that it occurs in the absence of antibiotics, and that
BlaR1 directly degrades BlaI, the gene repressor of the system. Furthermore,
we disclosed that this proteolytic activity is metal ion-dependent
and that it is not modulated directly by acylation of the sensor domain
by β-lactam antibiotics