Bacterial cell division requires recruitment of peptidoglycan (PG) synthases to the division site by the tubulin homologue, FtsZ. Septal PG synthases promote septum growth. FtsZ treadmilling is proposed to drive the processive movement of septal PG synthases and septal constriction in some bacteria; however, the precise mechanisms spatio-temporally regulating PG synthase movement and activity and FtsZ treadmilling are poorly understood. Here using single-molecule imaging of division proteins in the Gram-positive pathogen Staphylococcus aureus, we showed that the septal PG synthase complex FtsW/PBP1 and its putative activator protein, DivIB, move with similar velocity around the division site. Impairing FtsZ treadmilling did not affect FtsW or DivIB velocities or septum constriction rates. Contrarily, PG synthesis inhibition decelerated or stopped directional movement of FtsW and DivIB, and septum constriction. Our findings suggest that a single population of processively moving FtsW/PBP1 associated with DivIB drives cell constriction independently of FtsZ treadmilling in S. aureus.

细菌细胞分裂需要微管蛋白同源物 FtsZ 将肽聚糖 (PG) 合酶募集到分裂位点。隔膜 PG 合酶促进隔膜生长。FtsZ 踏车被认为可以驱动某些细菌中隔膜 PG 合酶和隔膜收缩的持续运动；然而，人们对时空调节 PG 合酶运动和活性以及 FtsZ 跑步的精确机制知之甚少。在这里，我们利用革兰氏阳性病原体金黄色葡萄球菌中分裂蛋白的单分子成像，发现隔膜 PG 合酶复合物 FtsW/PBP1 及其假定的激活蛋白 DivIB 在分裂位点周围以相似的速度移动。损害 FtsZ 跑步机不会影响 FtsW 或 DivIB 速度或隔膜收缩率。相反，PG 合成抑制会减慢或停止 FtsW 和 DivIB 的定向运动以及隔膜收缩。我们的研究结果表明，在金黄色葡萄球菌中，与 DivIB 相关的单个持续移动的 FtsW/PBP1 群体独立于 FtsZ 跑步驱动细胞收缩。