Persistence, the stress-tolerant state, is arguably the most vital phenotype since nearly all cells experience nutrient stress, which causes a sub-population to become dormant. However, how persister cells wake to reconstitute infections is not understood well. Here, using single-cell observations, we determined that Escherichia coli persister cells resuscitate primarily when presented with specific carbon sources, rather than spontaneously. In addition, we found that the mechanism of persister cell waking is through sensing nutrients by chemotaxis and phosphotransferase membrane proteins. Furthermore, nutrient transport reduces the level of secondary messenger cAMP through enzyme IIA; this reduction in cAMP levels leads to ribosome resuscitation and rescue. Resuscitating cells also immediately commence chemotaxis toward nutrients, although flagellar motion is not required for waking. Hence, persister cells wake by perceiving nutrients via membrane receptors that relay the signal to ribosomes via the secondary messenger cAMP, and persisters wake and utilize chemotaxis to acquire nutrients.

持久性，即耐压力状态，可以说是最重要的表型，因为几乎所有细胞都经历营养胁迫，这会导致亚群进入休眠状态。但是，人们对持久性细胞如何唤醒以重构感染的认识还不清楚。在这里，使用单细胞观察，我们确定大肠杆菌当存在特定的碳源时，持久性细胞主要是复苏，而不是自发的。此外，我们发现持久性细胞苏醒的机制是通过趋化性和磷酸转移酶膜蛋白来感知营养。此外，营养物质的运输通过酶IIA降低了次级信使cAMP的水平。cAMP水平的降低导致核糖体复苏和抢救。尽管苏醒不需要鞭毛运动，但复苏的细胞也可立即开始趋向营养。因此，持久性细胞通过经由膜受体感知营养而醒来，该膜受体通过次级信使cAMP将信号传递给核糖体，持久性醒并利用趋化性获取营养。