Arenicin-1-induced apoptosis-like response requires RecA activation and hydrogen peroxide against Escherichia coli.
Curr Genet
; 65(1): 167-177, 2019 Feb.
Article
em En
| MEDLINE
| ID: mdl-29881920
ABSTRACT
Arenicin-1, a 21-mer antimicrobial peptide exerts significant broad-spectrum antimicrobial activity with membrane-active mechanisms. However, owing to multiple mechanisms of cell death, the antibacterial mechanism of arenicin-1 requires detailed analysis. In the present study, arenicin-1-treated bacteria underwent an apoptosis-like response, which was mechanistically and morphologically similar to eukaryotic apoptosis. Changes in the physiological status of arenicin-1-treated bacterial cells involved accumulation of reactive oxygen species, imbalance of intracellular calcium gradients, disruption of membrane potential, bacterial caspase-like protein activation, and DNA damage. In arenicin-1-induced apoptosis-like death, autocleavage of LexA was observed because of the activation of the caspase-like activity of RecA. Additionally, typical reactive oxygen species such as superoxide, hydrogen peroxide, and hydroxyl radicals, were scavenged in arenicin-1-treated cells to assess the role of specific reactive oxygen species. Scavenging of hydrogen peroxide interfered with the activity of arenicin-1 in Escherichia coli, whereas the superoxide and hydroxyl radicals level did not affect arenicin-1-induced apoptosis-like death activity. Furthermore, inhibition of Fenton reaction attenuated apoptosis-like response. In conclusion, arenicin-1-induced apoptosis like death requires SOS response proteins and is mediated by hydrogen peroxide and Fenton reaction in E. coli. Arenicin-1 may be a representative antimicrobial peptide with potent apoptotic response against E. coli.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Recombinases Rec A
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Resposta SOS em Genética
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Apoptose
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Peptídeos Catiônicos Antimicrobianos
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Proteínas de Escherichia coli
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Escherichia coli
Idioma:
En
Revista:
Curr Genet
Ano de publicação:
2019
Tipo de documento:
Article