Imperial College London

ProfessorGadFrankel

Faculty of Natural SciencesDepartment of Life Sciences

Professor of Molecular Pathogenesis
 
 
 
//

Contact

 

+44 (0)20 7594 5253g.frankel

 
 
//

Location

 

1.46Flowers buildingSouth Kensington Campus

//

Summary

 

Publications

Citation

BibTex format

@article{Sandu:2017:10.1128/IAI.00244-17,
author = {Sandu, P and Crepin, VF and Drechsler, H and McAinsh, AD and Frankel, G and Berger, CN},
doi = {10.1128/IAI.00244-17},
journal = {Infect Immun},
title = {The Enterohemorrhagic Escherichia coli Effector EspW Triggers Actin Remodeling in a Rac1-Dependent Manner.},
url = {http://dx.doi.org/10.1128/IAI.00244-17},
volume = {85},
year = {2017}
}

RIS format (EndNote, RefMan)

TY  - JOUR
AB - Enterohemorrhagic Escherichia coli (EHEC) is a diarrheagenic pathogen that colonizes the gut mucosa and induces attaching-and-effacing lesions. EHEC employs a type III secretion system (T3SS) to translocate 50 effector proteins that hijack and manipulate host cell signaling pathways, which allow bacterial colonization and subversion of immune responses and disease progression. The aim of this study was to characterize the T3SS effector EspW. We found espW in the sequenced O157:H7 and non-O157 EHEC strains as well as in Shigella boydii Furthermore, a truncated version of EspW, containing the first 206 residues, is present in EPEC strains belonging to serotype O55:H7. Screening a collection of clinical EPEC isolates revealed that espW is present in 52% of the tested strains. We report that EspW modulates actin dynamics in a Rac1-dependent manner. Ectopic expression of EspW results in formation of unique membrane protrusions. Infection of Swiss cells with an EHEC espW deletion mutant induces a cell shrinkage phenotype that could be rescued by Rac1 activation via expression of the bacterial guanine nucleotide exchange factor, EspT. Furthermore, using a yeast two-hybrid screen, we identified the motor protein Kif15 as a potential interacting partner of EspW. Kif15 and EspW colocalized in cotransfected cells, while ectopically expressed Kif15 localized to the actin pedestals following EHEC infection. The data suggest that Kif15 recruits EspW to the site of bacterial attachment, which in turn activates Rac1, resulting in modifications of the actin cytoskeleton that are essential to maintain cell shape during infection.
AU - Sandu,P
AU - Crepin,VF
AU - Drechsler,H
AU - McAinsh,AD
AU - Frankel,G
AU - Berger,CN
DO - 10.1128/IAI.00244-17
PY - 2017///
TI - The Enterohemorrhagic Escherichia coli Effector EspW Triggers Actin Remodeling in a Rac1-Dependent Manner.
T2 - Infect Immun
UR - http://dx.doi.org/10.1128/IAI.00244-17
UR - https://www.ncbi.nlm.nih.gov/pubmed/28630074
VL - 85
ER -