MurAA is required for intrinsic cephalosporin resistance of Enterococcus faecalis.
MurAA is required for intrinsic cephalosporin resistance of Enterococcus faecalis.
复制标题
MurAA 是粪肠球菌固有头孢菌素耐药性所必需的。
DOI：
10.1128/aac.05984-11
复制
发表时间：
2012
影响因子：
4.9
通讯作者：
Kristich,ChristopherJ
中科院分区：
文献类型：
--
作者：
Vesic,Dusanka;Kristich,ChristopherJ
Enterococcus faecalis is a low-GC Gram-positive bacterium that is intrinsically resistant to cephalosporins, antibiotics that target cell wall biosynthesis. To probe the mechanistic basis for intrinsic resistance, a library of transposon mutants was screened to identify E. faecalis strains that are highly susceptible to ceftriaxone, revealing a transposon mutant with a disruption inmurAA. murAAis predicted to encode a UDP-N-acetylglucosamine 1-carboxyvinyl transferase that catalyzes the first committed step in peptidoglycan synthesis: phosphoenolpyruvate (PEP)-dependent conversion of UDP-N-acetylglucosamine to UDP-N-acetylglucosamine-enolpyruvate. In-frame deletion ofmurAA, but not its homolog in the E. faecalis genome (murAB), led to increased susceptibility of E. faecalis to cephalosporins. Furthermore, expression ofmurAAenhanced cephalosporin resistance in an E. faecalis mutant lacking IreK (formerly PrkC), a key kinase required for cephalosporin resistance. Further genetic analysis revealed that MurAA catalytic activity is necessary but not sufficient for this role. Collectively, our data indicate that MurAA and MurAB have distinct roles in E. faecalis physiology and suggest that MurAA possesses a unique property or activity that enables it to enhance intrinsic resistance of E. faecalis to cephalosporins.
