Lewis Richard J
Institute for Cell and Molecular Biosciences, Newcastle University, Newcastle Upon Tyne, NE2 4HH, UK.
Mol Microbiol. 2017 Mar;103(6):913-918. doi: 10.1111/mmi.13612. Epub 2017 Jan 12.
Peptidoglycan (PG), an essential stress-bearing component of the bacterial cell wall, is synthesised by penicillin binding proteins (PBPs). PG synthesis at the cell division septum is necessary for constructing new poles of progeny cells, and cells cannot elongate without inserting new PG in the side-wall. The cell division regulator GpsB appears to co-ordinate PG synthesis at the septum during division and at the side-wall during elongation in rod-shaped and ovococcoid Gram-positive bacteria. How the control over PG synthesis is exerted is unknown. In this issue of Molecular Microbiology, Rued et al. show that in pneumococci GpsB forms complexes with PBP2a and PBP2b, and that deletion or depletion of GpsB prevents closure of the septal ring that in itself is PBP2x-dependent. Loss of GpsB can be suppressed by spontaneous mutations, including within the gene encoding the only PP2C Ser/Thr phosphatase in Streptococcus pneumoniae, indicating that GpsB plays a key - but unknown - role in protein phosphorylation in pneumococci. Rued et al. combine phenotypic and genotypic analyses of mutant strains that suggest discrepancies in the literature concerning GpsB might have arisen from accumulation of unidentified suppressors, highlighting the importance and power of strain validation and whole genome sequencing in this context.
肽聚糖（PG）是细菌细胞壁中一种重要的承受压力的成分，由青霉素结合蛋白（PBPs）合成。在细胞分裂隔膜处合成PG对于构建子代细胞的新极是必要的，并且细胞如果不在侧壁插入新的PG就无法伸长。细胞分裂调节因子GpsB似乎在杆状和卵球形革兰氏阳性细菌的分裂过程中协调隔膜处的PG合成以及伸长过程中侧壁处的PG合成。目前尚不清楚对PG合成的控制是如何实现的。在本期《分子微生物学》中，鲁德等人表明，在肺炎链球菌中，GpsB与PBP2a和PBP2b形成复合物，并且GpsB的缺失或耗尽会阻止隔膜环的闭合，而隔膜环本身依赖于PBP2x。GpsB的缺失可以通过自发突变来抑制，包括在编码肺炎链球菌中唯一的PP2C丝氨酸/苏氨酸磷酸酶的基因内，这表明GpsB在肺炎链球菌的蛋白质磷酸化中起着关键但未知的作用。鲁德等人结合了突变菌株的表型和基因型分析，表明文献中关于GpsB的差异可能是由于未鉴定的抑制子积累所致，突出了在这种情况下菌株验证和全基因组测序的重要性和作用。
