School of Life Sciences, BK21 Plus KNU Creative BioResearch Group, Kyungpook National University, Daegu, 41566, Korea.
Department of Agricultural Biology, National Academy of Agricultural Science, RDA, Wanju, 55365, Republic of Korea.
Appl Microbiol Biotechnol. 2019 Feb;103(3):1417-1427. doi: 10.1007/s00253-018-9561-9. Epub 2018 Dec 15.
Periplanetasin-2 is a 15-mer antimicrobial peptide (AMP), derived from the American cockroach Periplaneta americana. This novel AMP exhibits potent antibacterial effect against several pathogenic bacteria including Escherichia coli. Distinct from the targeting cell membrane, which is the general antibacterial mechanism of AMP, periplanetasin-2 exerts its antibacterial activity via apoptosis-like death, which is physiologically and mechanistically similar to eukaryotic apoptosis. E. coli cells treated with periplanetasin-2 showed features of apoptosis in a concentration-dependent manner, such as membrane depolarization, DNA fragmentation, caspase-like protein activation, and phosphatidylserine externalization. These physiological changes were attenuated by pretreatment with the reactive oxygen species (ROS) scavenger, which demonstrates that periplanetasin-2 induced apoptosis-like death in E. coli by generating ROS. In addition, periplantasin-2-induced apoptotic death was affected by SOS response components. In the absence of RecA, an essential protein for SOS response, apoptosis did not occur and the antibacterial activity of periplanetasin-2 was decreased. In contrast, deletion of the SOS gene dinF caused higher ROS accumulation and apoptotic features were detected. Collectively, these results indicate that the antibacterial mechanism of periplanetasin-2 is ROS-induced apoptosis-like death, which requires RecA for proceeding it, and the role of DinF is assumed to contribute to the ROS defense SOS response.
periplanetasin-2 是一种 15 肽抗菌肽 (AMP),来源于美洲大蠊 Periplaneta americana。这种新型 AMP 对多种致病菌具有强大的抗菌作用,包括大肠杆菌。与靶向细胞膜的一般 AMP 抗菌机制不同,periplanetasin-2 通过细胞凋亡样死亡发挥其抗菌活性,这种死亡在生理和机制上与真核细胞凋亡相似。用 periplanetasin-2 处理的大肠杆菌细胞表现出浓度依赖性的凋亡特征,如细胞膜去极化、DNA 片段化、半胱天冬酶样蛋白激活和磷脂酰丝氨酸外翻。这些生理变化通过用活性氧 (ROS) 清除剂预处理得到减弱,表明 periplanetasin-2 通过生成 ROS 诱导大肠杆菌发生细胞凋亡样死亡。此外,periplantasin-2 诱导的凋亡死亡受 SOS 反应成分的影响。在缺乏 SOS 反应必需蛋白 RecA 的情况下,不会发生细胞凋亡,periplanetasin-2 的抗菌活性降低。相比之下,缺失 SOS 基因 dinF 会导致更多的 ROS 积累,并检测到凋亡特征。总之,这些结果表明 periplanetasin-2 的抗菌机制是 ROS 诱导的细胞凋亡样死亡,需要 RecA 才能进行,DinF 的作用可能是有助于 ROS 防御 SOS 反应。