ArticlePLoS pathogens2018
Enteropathogenic E. coli relies on collaboration between the formin mDia1 and the Arp2/3 complex for actin pedestal biogenesis and maintenance.
Article in PLoS pathogens, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 27 citations in OpenAlex.
- Myosin IIA motor regulates attaching-effacing bacteria interactions with intestinal epithelium.Gut microbes · 2026Article
- Brush border intermicrovillar adhesion limits bacteria attachment to the small intestine brush border.bioRxiv : the preprint server for biology · 2025Article
- Please inhibit responsibly: Natural and synthetic actin toxins as useful tools in cell biology.Molecular biology of the cell · 2025Review
- Overexpressed Palladin Rescues Enteropathogenic E. coli (EPEC) Pedestal Lengths in ArpC2 Depleted Cells.Cytoskeleton (Hoboken, N.J.) · 2025Article
- Antagonistic Effects of Actin-Specific Toxins onBiomolecules · 2024Article
- Cytoskeletal mechanisms regulating attaching/effacing bacteria interactions with host cells: It takes a village to build the pedestal.BioEssays : news and reviews in molecular, cellular and developmental biology · 2024Review
- Pushing boundaries: mechanisms enabling bacterial pathogens to spread between cells.Infection and immunity · 2024Review
- Why put yourself on a pedestal? The pathogenic role of the A/E pedestal.Infection and immunity · 2024Review
- Antagonistic effects of actin-specific toxins onbioRxiv : the preprint server for biology · 2024Article
- Increased cross-presentation by dendritic cells and enhanced anti-tumour therapy using the Arp2/3 inhibitor CK666.British journal of cancer · 2023Article
- Distinct roles of the Chlamydia trachomatis effectors TarP and TmeA in the regulation of formin and Arp2/3 during entry.Journal of cell science · 2022Article
- Effects of lipoteichoic and arachidonic acids on the immune-regulatory mechanism of bovine mammary epithelial cells using multi-omics analysis.Frontiers in veterinary science · 2022Article
- Conserved actin machinery drives microtubule-independent motility and phagocytosis in Naegleria.The Journal of cell biology · 2020Article
- Staying out or Going in? The Interplay between Type 3 and Type 5 Secretion Systems in Adhesion and Invasion of Enterobacterial Pathogens.International journal of molecular sciences · 2020Review
- WHIMP links the actin nucleation machinery to Src-family kinase signaling during protrusion and motility.PLoS genetics · 2020Article
- Correlative light and scanning electron microscopy (CLSEM) for analysis of bacterial infection of polarized epithelial cells.Scientific reports · 2019Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Enteropathogenic and enterohemorrhagic E. coli (EPEC and EHEC) are closely related extracellular pathogens that reorganize host cell actin into "pedestals" beneath the tightly adherent bacteria. This pedestal-forming activity is both a critical step in pathogenesis, and it makes EPEC and EHEC useful models for studying the actin rearrangements that underlie membrane protrusions. To generate pedestals, EPEC relies on the tyrosine phosphorylated bacterial effector protein Tir to bind host adaptor proteins that recruit N-WASP, a nucleation-promoting factor that activates the Arp2/3 complex to drive actin polymerization. In contrast, EHEC depends on the effector EspFU to multimerize N-WASP and promote Arp2/3 activation. Although these core pathways of pedestal assembly are well-characterized, the contributions of additional actin nucleation factors are unknown. We investigated potential cooperation between the Arp2/3 complex and other classes of nucleators using chemical inhibitors, siRNAs, and knockout cell lines. We found that inhibition of formins impairs actin pedestal assembly, motility, and cellular colonization for bacteria using the EPEC, but not the EHEC, pathway of actin polymerization. We also identified mDia1 as the formin contributing to EPEC pedestal assembly, as its expression level positively correlates with the efficiency of pedestal formation, and it localizes to the base of pedestals both during their initiation and once they have reached steady state. Collectively, our data suggest that mDia1 enhances EPEC pedestal biogenesis and maintenance by generating seed filaments to be used by the N-WASP-Arp2/3-dependent actin nucleation machinery and by sustaining Src-mediated phosphorylation of Tir.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.