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首页> 外文期刊>Journal of bacteriology >Suppressor Mutations Linking gpsB with the First Committed Step of Peptidoglycan Biosynthesis in Listeria monocytogenes
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Suppressor Mutations Linking gpsB with the First Committed Step of Peptidoglycan Biosynthesis in Listeria monocytogenes

机译：连接gpsB与单核细胞增生性李斯特菌中肽聚糖生物合成的第一个第一步的抑制基因突变

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摘要

The cell division protein GpsB is a regulator of the penicillin binding protein A1 (PBP A1) in the Gram-positive human pathogen Listeria monocytogenes. Penicillin binding proteins mediate the last two steps of peptidoglycan biosynthesis as they polymerize and cross-link peptidoglycan strands, the main components of the bacterial cell wall. It is not known what other processes are controlled by GpsB. L. monocytogenes gpsB mutants are unable to grow at 42°C, but we observed that spontaneous suppressors correcting this defect arise on agar plates with high frequency. We here describe a first set of gpsB suppressors that mapped to the clpC and murZ genes. While ClpC is the ATPase component of the Clp protease, MurZ is a paralogue of the listerial UDP–N-acetylglucosamine (UDP-GlcNAc) 1-carboxyvinyltransferase MurA. Both enzymes catalyze the enolpyruvyl transfer from phosphoenolpyruvate to UDP-GlcNAc, representing the first committed step of peptidoglycan biosynthesis. We confirmed that clean deletion of the clpC or murZ gene suppressed the ΔgpsB phenotype. It turned out that the absence of either gene leads to accumulation of MurA, and we show that artificial overexpression of MurA alone was sufficient for suppression. Inactivation of other UDP-GlcNAc-consuming pathways also suppressed the heat-sensitive growth of the ΔgpsB mutant, suggesting that an increased influx of precursor molecules into peptidoglycan biosynthesis can compensate for the lack of GpsB. Our results support a model according to which PBP A1 becomes misregulated and thus toxic in the absence of GpsB due to unproductive consumption of cell wall precursor molecules.
机译：细胞分裂蛋白GpsB是革兰氏阳性人类病原体单核细胞增生李斯特氏菌中青霉素结合蛋白A1（PBP A1）的调节剂。青霉素结合蛋白在聚合和交联肽聚糖链（细菌细胞壁的主要成分）时介导肽聚糖生物合成的最后两个步骤。尚不知道GpsB还控制哪些其他进程。单核细胞增生李斯特氏菌 gpsB 突变体无法在42°C下生长，但是我们观察到，在琼脂平板上出现的自发抑制因子会纠正这种缺陷，发生频率很高。我们在这里描述了映射到 clpC 和 murZ 基因的第一组 gpsB 抑制子。 ClpC是Clp蛋白酶的ATPase成分，而MurZ是利斯特型UDP- N -乙酰氨基葡糖（UDP-GlcNAc）1-羧基乙烯基转移酶MurA的类似物。两种酶都催化从磷酸烯醇丙酮酸酯到烯丙基丙酮酸酯向UDP-GlcNAc的转移，这代表肽聚糖生物合成的第一步。我们确认 clpC 或 murZ 基因的干净删除抑制了Δ gpsB 表型。事实证明，任何一个基因的缺失都会导致MurA的积累，并且我们证明了单独人工表达MurA足以抑制。其他UDP-GlcNAc消耗途径的失活也抑制了Δ gpsB 突变体的热敏生长，表明前体分子向肽聚糖生物合成中的大量流入可以弥补GpsB的缺乏。我们的结果支持了一种模型，根据该模型，由于细胞壁前体分子的非生产性消耗，PBP A1在GpsB缺失的情况下变得失控，因此具有毒性。

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