 deletion (and tolerates prkA deletion) would provide strong evidence for the model. Were such experiments attempted? If not, they should be considered to strengthen the conclusions.  0\) To support the conclusions, analysis PG precursor levels appear necessary in this case. The entire model is based on protein stability but the functional consequences of this on cell viability and PG homeostasis have not been studied here. The relationship with resistance to cell wall targeting antibiotics is anecdotal. Perhaps assessing the thickness of the cell wall would provide more supporting information.  