The small size of bacterial cells necessitates rapid adaption to sudden environmental changes. In Bdellovibrio bacteriovorus, an obligate predator of bacteria common in oligotrophic environments, the non-replicative, highly motile attack phase (AP) cell must invade a prey to ensure replication. AP cells swim fast and respire at high rates, rapidly consuming their own contents. How the predator survives in the absence of prey is unknown. We show that starvation for prey significantly alters swimming patterns and causes exponential decay in prey-searching cells over hours, until population-wide swim-arrest. Swim-arrest is accompanied by changes in energy metabolism, enabling rapid swim-reactivation upon introduction of prey or nutrients, and a sweeping change in gene expression and gene regulation that largely differs from those of the paradigmatic stationary phase. Swim-arrest is costly as it imposes a fitness penalty in the form of delayed growth. We track the control of the swim arrest-reactivation process to cyclic-di-GMP (CdG) effectors, including two motility brakes. CRISPRi transcriptional inactivation, and in situ localization of the brakes to the cell pole, demonstrated their essential role for effective survival under prey-induced starvation. Thus, obligate predators evolved a unique CdG-controlled survival strategy, enabling them to sustain their uncommon lifestyle under fluctuating prey supply.

细菌细胞体积小，需要快速适应突然的环境变化。在噬菌蛭弧菌（一种常见于寡营养环境中的细菌的专性捕食者）中，非复制性、高度活动性的攻击期（AP）细胞必须侵入猎物以确保复制。 AP 细胞快速游动并以高速率呼吸，迅速消耗其自身内容物。捕食者如何在没有猎物的情况下生存尚不清楚。我们发现，对猎物的饥饿会显着改变游泳模式，并导致搜索猎物的细胞在数小时内呈指数衰减，直到整个种群的游泳停滞。游泳停滞伴随着能量代谢的变化，在引入猎物或营养物后能够快速重新激活游泳，并且基因表达和基因调控发生彻底的变化，这与范式静止期的变化有很大不同。游泳被捕的代价高昂，因为它会以生长延迟的形式对健康造成影响。我们跟踪对环二 GMP (CdG) 效应器的游泳停滞-重新激活过程的控制，包括两个运动制动器。 CRISPRi 转录失活以及制动装置在细胞极的原位定位，证明了它们对于在猎物诱导的饥饿下有效生存的重要作用。因此，专性捕食者进化出了一种独特的 CdG 控制的生存策略，使它们能够在猎物供应波动的情况下维持不寻常的生活方式。