It was speculated that the increase of the UDP-GlcNAc pool observed with chloramphenicol can modulate the residual PEP:UDP-GlcNAc-enolpyruvate activity of fosfomycin-treated cells. This provided an explanation on how chloramphenicol can insure the formation of enough UDP-MurNAc-pentapeptide to sustain peptidoglycan synthesis at a rate that will antagonize fosfomycin-induced lysis.
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