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变形链球菌中假定的自溶素调节因子LytR在细胞分裂中起作用,并受生长阶段调控。

The putative autolysin regulator LytR in Streptococcus mutans plays a role in cell division and is growth-phase regulated.

作者信息

Chatfield Christa H, Koo Hyun, Quivey Robert G

机构信息

in the Aab Institute for Biomedical Sciences and Department of Microbiology and Immunology, University of Rochester, Rochester, NY 14642, USA.

Eastman Department of Dentistry, University of Rochester, Rochester, NY 14642, USA.

出版信息

Microbiology (Reading). 2005 Feb;151(Pt 2):625-631. doi: 10.1099/mic.0.27604-0.

DOI:10.1099/mic.0.27604-0
PMID:15699211
Abstract

Streptococcus mutans is the primary odontopathogen present in supragingival plaque and causes the oral disease known as dental caries. Colonization of the oral cavity by S. mutans requires the bacteria to adhere to the tooth surface and occurs by both sucrose-dependent and -independent mechanisms. Sucrose-independent adhesion of S. mutans in vitro has been shown to involve an ORF (ORF0317) encoding a homologue (39 %) to LytR, a regulator of autolysin activity in Bacillus subtilis. The protein encoded by ORF0317, LytR, belongs to the LytR/CpsA/Psr protein family. This family has a putative role in cell-wall structural maintenance, possibly through autolysin regulation. Autolysins have also been shown to be important in surface adhesion in Lactococcus lactis and in the pathogenic properties of Streptococcus pneumoniae. To investigate the role of autolysins in the adhesion and pathogenesis of S. mutans, a LytR mutant was constructed. The mutant grows in long chains, which may indicate a defect in cell division. Further experiments with the mutant strain show increased autolytic activity, indicating that LytR attenuates S. mutans autolytic activity, possibly through regulation of the expression of autolytic enzymes. No defect in cell-to-surface adherence or biofilm growth was seen in the LytR mutant. However, a connection between cell growth phase and transcription of lytR was found.

摘要

变形链球菌是龈上菌斑中主要的致龋病原体,可引发名为龋齿的口腔疾病。变形链球菌在口腔内的定植需要细菌粘附于牙齿表面,这一过程通过依赖蔗糖和不依赖蔗糖的机制发生。体外实验表明,变形链球菌不依赖蔗糖的粘附涉及一个开放阅读框(ORF0317),该开放阅读框编码一种与枯草芽孢杆菌自溶素活性调节因子LytR同源性为39%的蛋白。由ORF0317编码的蛋白LytR属于LytR/CpsA/Psr蛋白家族。该家族可能通过自溶素调节在细胞壁结构维持中发挥作用。自溶素在乳酸乳球菌的表面粘附中以及肺炎链球菌的致病特性中也被证明具有重要作用。为了研究自溶素在变形链球菌粘附和致病机制中的作用,构建了一个LytR突变体。该突变体呈长链状生长,这可能表明细胞分裂存在缺陷。对突变菌株的进一步实验显示自溶活性增加,这表明LytR可能通过调节自溶酶的表达来减弱变形链球菌的自溶活性。在LytR突变体中未观察到细胞与表面粘附或生物膜生长方面的缺陷。然而,发现了细胞生长阶段与lytR转录之间的联系。

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