TY - JOUR
T1 - To hunt or to rest
T2 - prey depletion induces a novel starvation survival strategy in bacterial predators
AU - Sathyamoorthy, Rajesh
AU - Kushmaro, Yuval
AU - Rotem, Or
AU - Matan, Ofra
AU - Kadouri, Daniel E.
AU - Huppert, Amit
AU - Jurkevitch, Edouard
N1 - Publisher Copyright:
© 2020, The Author(s), under exclusive licence to International Society for Microbial Ecology.
PY - 2021/1
Y1 - 2021/1
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=85090241833&partnerID=8YFLogxK
U2 - 10.1038/s41396-020-00764-2
DO - 10.1038/s41396-020-00764-2
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C2 - 32884113
AN - SCOPUS:85090241833
SN - 1751-7362
VL - 15
SP - 109
EP - 123
JO - ISME Journal
JF - ISME Journal
IS - 1
ER -