ArticlePloS one2013
The N-terminal domain of EspF induces host cell apoptosis after infection with enterohaemorrhagic Escherichia coli O157:H7.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 23 citations in OpenAlex.
- Transcriptomic and proteomic analysis of the virulence inducing effect of ciprofloxacin on enterohemorrhagic Escherichia coli.PloS one · 2024Article
- Reprogramming of Cell Death Pathways by Bacterial Effectors as a Widespread Virulence Strategy.Infection and immunity · 2022Review
- EspF of EnterohemorrhagicFrontiers in microbiology · 2022Article
- AnFrontiers in microbiology · 2021Article
- Polyphosphate Kinase 1 Is a Pathogenesis Determinant in EnterohemorrhagicFrontiers in microbiology · 2021Article
- Clever Cooperation: Interactions Between EspF and Host Proteins.Frontiers in microbiology · 2018Review
- The EspF N-Terminal of EnterohemorrhagicFrontiers in cellular and infection microbiology · 2017Article
- Bacterial secreted effectors and caspase-3 interactions.Cellular microbiology · 2014Review
- Enterohemorrhagic Escherichia coli hemolysin employs outer membrane vesicles to target mitochondria and cause endothelial and epithelial apoptosis.PLoS pathogens · 2013Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Enterohemorrhagic Escherichia coli (EHEC) employs a type III secretion system (TTSS) to export the translocator and effector proteins required for mucosal colonization. As an important bacterial effector protein in locus of enterocyte effacement four, the EspF protein causes F-actin filament aggregations to form attaching and effacing (A/E) lesions, and induces the destruction of brush-border microvilli and cytoskeletal rearrangements to form pedestals. However, the molecular pathogenesis of A/E lesions due to EHEC O157:H7 infection is unclear. In this study, we constructed an espF-deficient mutant (ΔespF) with a 162-bp deletion in the N-terminal domain by using overlap extension PCR. The results showed that EHEC EspF translocated into intestinal epithelial cells, targeted mitochondria and induced apoptosis. The ΔespF mutant, compared to EHEC prototype Guangzhou strain, had lower cell attachment and effacement abilities, lower caspase-9/3 and lactate dehydrogenase levels, lower bacterial adhesion, weaker mitochondria apoptosis, and a higher mouse survival rate. Our results demonstrate the probable function of the EspF N-terminal domain, which targets mitochondria and binds mitochondria heat shock protein 70 to induce cell apoptosis via A/E lesions. These findings may be invaluable in clarifying the molecular pathogenesis of EspF of EHEC O157:H7.
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