重新定义磷壁酸在海氏肠球菌β-内酰胺抗性和细胞自溶中的作用。
Redefining the role of psr in beta-lactam resistance and cell autolysis of Enterococcus hirae.
作者信息
Sapunaric Frédéric, Franssen Christine, Stefanic Patrick, Amoroso Ana, Dardenne Olivier, Coyette Jacques
机构信息
Department of Molecular Biology and Microbiology, School of Medicine, Tufts University, Boston, Massachusetts 02111, USA.
出版信息
J Bacteriol. 2003 Oct;185(20):5925-35. doi: 10.1128/JB.185.20.5925-5935.2003.
The contribution of penicillin-binding protein 5 (PBP5) and the PBP5 synthesis repressor (Psr) to the beta-lactam resistance, growth, and cell autolysis of wild-type strain ATCC 9790 and resistant strain R40 of Enterococcus hirae was investigated by disruption or substitution of the corresponding pbp5 and psr genes by Campbell-type recombination. The resulting modifications were confirmed by hybridization and PCR. The low susceptibility of E. hirae to beta-lactams was confirmed to be largely dependent on the presence of PBP5. However, against all expectations, inactivation of psr in ATCC 9790 or complementation of R40 cells with psr did not modify the susceptibility to benzylpenicillin or the growth and cell autolysis rates. These results indicated that the psr gene does not seem to be involved in the regulation of PBP5 synthesis and consequently in beta-lactam resistance or in the regulation of cell autolysis in E. hirae.
通过坎贝尔型重组对相应的pbp5和psr基因进行破坏或替换，研究了青霉素结合蛋白5（PBP5）和PBP5合成阻遏物（Psr）对平肠球菌野生型菌株ATCC 9790和耐药菌株R40的β-内酰胺抗性、生长及细胞自溶的作用。通过杂交和PCR对产生的修饰进行了确认。已证实平肠球菌对β-内酰胺的低敏感性很大程度上取决于PBP5的存在。然而，出乎意料的是，ATCC 9790中psr的失活或用psr对R40细胞进行互补，并未改变对苄青霉素的敏感性或生长及细胞自溶速率。这些结果表明，psr基因似乎不参与PBP5合成的调控，因此也不参与平肠球菌中β-内酰胺抗性或细胞自溶的调控。
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