Evidence that CT694 is a novel Chlamydia trachomatis T3S substrate capable of functioning during invasion or early cycle development.
Evidence that CT694 is a novel Chlamydia trachomatis T3S substrate capable of functioning during invasion or early cycle development.
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DOI：
10.1111/j.1365-2958.2009.06732.x
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发表时间：
2009-06
影响因子：
3.6
通讯作者：
Fields KA
中科院分区：
文献类型：
--
作者：
Hower S;Wolf K;Fields KA
青霉素结合蛋白(PBPs)催化细胞壁肽聚糖的合成。金黄色葡萄球菌的PBP1是一种高相对分子质量的单功能转肽酶(TPase)，以前对条件突变体的研究表明，该蛋白对细菌的生长和生存是必不可少的：在PBP1耗尽的细胞中，细胞停止分裂，但体积继续扩大，伴随着活力的迅速丧失。此外，在PBP1耗尽的情况下产生的细胞壁似乎具有正常的成分。我们在这里描述了第二个PBP1突变体的构建，在该突变体中，TPase结构域的活性部位被灭活。用突变蛋白取代野生型PBP1的细胞能够启动和完成分裂，并经历至少一到两次细胞分裂，之后生长停止，伴随着细胞分离的抑制，自溶系统转录的下调和细胞壁的产生，单体和二聚体多肽的比例增加，多肽寡聚体的减少。PBP1似乎在金黄色葡萄球菌的细胞周期中扮演着双重角色：作为一种启动分离所需的蛋白质，也作为一种转肽酶，在细胞分裂结束时产生细胞分离的关键信号。
Penicillin-binding proteins (PBPs) catalyze the synthesis of cell wall peptidoglycan. PBP1of Staphylococcus aureus is a high molecular weight monofunctional transpeptidase (TPase) and previous studies with a conditional mutant showed that this protein was essential for bacterial growth and survival: cells in which PBP1 was depleted stopped dividing but continued to enlarge in size, accompanied by rapid loss of viability. Also, cell walls produced under PBP1 depletion appeared to have normal composition. We describe here construction of a second PBP1 mutant in which the active site of TPase domain was inactivated. Cells in which the wild type PBP1 was replaced by the mutant protein were able to initiate and complete septa and undergo at least one or two cell divisions after which growth stopped accompanied by inhibition of cell separation, down-regulation in the transcription of the autolytic system and production of cell walls with increased proportion of monomeric and dimeric muropeptides and decrease in muropeptide oligomers. PBP1 seems to perform a dual role in the cell cycle of S. aureus: as a protein required for the initiation of septation and also as a transpeptidase that generates a critical signal for cell separation at the end of cell division.
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影响因子：
3.6
作者：
Fields, KA;Mead, DJ;Hackstadt, T
通讯作者：
Hackstadt, T
影响因子：
3.6
作者：
Fields, KA;Hackstadt, T
通讯作者：
Hackstadt, T
影响因子：
4
作者：
Grieshaber, SS;Grieshaber, NA;Hackstadt, T
通讯作者：
Hackstadt, T
影响因子：
3.6
作者：
Day, JB;Plano, GV
通讯作者：
Plano, GV
影响因子：
4.8
作者：
Hohaus, A;Person, V;Haase, H
通讯作者：
Haase, H