Antimicrobial peptides are one of the promising substitutes for conventional antibiotics. To examine their potential usefulness for controlling bacterial infections, the present study aimed to determine the induction of the self-destruction of Escherichia coli mediated by bac8c, which was modified from template peptide bactenecin. The potential of bac8c (RIWVIWRR) was reflected by the change in physiological following exposure, which led to the accumulation of reactive oxygen species (ROS) with an imbalance in the antioxidant system and damage to the intracellular lipids. In addition, bac8c-mediated death exhibited typical features to bacterial apoptosis-like death (ALD). The pathway was not enhanced in the absence of autocleavage of RecA and LexA, the SOS response proteins. We observed that elevated levels of intracellular ROS induced ALD, but this effect was insufficient before preceding RecA activation and LexA autocleavage. Furthermore, dinF, which encodes a member of the toxic compound extrusion (MATE) family, was evaluated to examine the role of the ALD pathway. dinF protein was required to accelerate the ALD-mediated bac8c in combination with RecA. Taken together, bac8c-mediated cell death underlies the severe SOS response, leading to RecA activation, LexA proteolysis, and dinF overexpression. Since then, overproduction of intracellular ROS facilitated the cell death.

抗菌肽是常规抗生素的有前途的替代品之一。为了检查它们对控制细菌感染的潜在作用，本研究旨在确定诱导大肠杆菌自我毁灭的能力。由bac8c介导的bac8c，它是由模板肽细菌素修饰的。bac8c（RIWVIWRR）的潜力通过暴露后的生理变化反映出来，这导致活性氧（ROS）积累，抗氧化剂系统失衡，破坏了细胞内脂质。此外，bac8c介导的死亡表现出细菌凋亡样死亡（ALD）的典型特征。在没有SOS反应蛋白RecA和LexA自动裂解的情况下，该途径没有得到增强。我们观察到细胞内ROS水平升高会诱发ALD，但在RecA激活和LexA自动裂解之前，这种作用是不足的。此外，dinF评估了编码有毒化合物挤出（MATE）家族成员的，以检查ALD途径的作用。需要dinF蛋白与RecA结合来加速ALD介导的bac8c。总之，bac8c介导的细胞死亡是严重的SOS反应的基础，导致RecA激活，LexA蛋白水解和dinF过表达。从那以后，细胞内ROS的过量产生促进了细胞死亡。