Imperial College London

ProfessorPaulLangford

Faculty of MedicineDepartment of Infectious Disease

Professor of Paediatric Infectious Diseases
 
 
 
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Contact

 

+44 (0)20 7594 3359p.langford Website

 
 
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Location

 

236Wright Fleming WingSt Mary's Campus

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Summary

 

Publications

Citation

BibTex format

@article{Edwards-Jones:2004:10.1099/mic.0.26840-0,
author = {Edwards-Jones, B and Langford, PR and Kroll, JS and Yu, J},
doi = {10.1099/mic.0.26840-0},
journal = {Microbiology},
pages = {1079--1084},
title = {The role of the Shigella flexneri yihE gene in LPS synthesis and virulence},
url = {http://dx.doi.org/10.1099/mic.0.26840-0},
volume = {150},
year = {2004}
}

RIS format (EndNote, RefMan)

TY  - JOUR
AB - Previously, the authors have shown that inactivation of Shigella flexneri yihE, a gene of unknown function upstream of dsbA, which encodes a periplasmic disulphide catalyst, results in a global change of gene expression. Among the severely down-regulated genes are galETKM, suggesting that the yihE mutant, Sh54, may inefficiently produce the UDP-glucose and UDP-galactose required for LPS synthesis. This paper demonstrates that LPS synthesis in Sh54 is impaired. As a result, Sh54 is unable to polymerize host cell actin, due to aberrant localization of IcsA, or to cause keratoconjunctivitis in guinea pigs. Furthermore, Sh54 is more sensitive to some antimicrobial agents, and exhibits epithelial cytotoxicity characteristic of neither wild-type nor dsbA mutants. Supplying galETK in trans restores LPS synthesis and corrects all the defects. Hence, it is clear that the Shigella yihE gene is important not only in regulating global gene expression, as shown previously, but also in virulence through LPS synthesis via regulating the expression of the galETK operon. © 2004 SGM.
AU - Edwards-Jones,B
AU - Langford,PR
AU - Kroll,JS
AU - Yu,J
DO - 10.1099/mic.0.26840-0
EP - 1084
PY - 2004///
SN - 1350-0872
SP - 1079
TI - The role of the Shigella flexneri yihE gene in LPS synthesis and virulence
T2 - Microbiology
UR - http://dx.doi.org/10.1099/mic.0.26840-0
VL - 150
ER -