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research
The HicA toxin from Burkholderia pseudomallei has a role in persister cell formation
Authors
Aaron Butt
Ahmad
+61 more
Bardiaux
Bhattacharya
Bigger
Blower
Butt
Christopher Williams
Claudia M. Hemsley
Currie
Delaglio
Doreleijers
Dörr
Fauvart
Fiebig
Gerdes
Gerdes
Goeders
Goodyear
Hayes
Heeb
Ichiyanagi
Joers
Jorgensen
Keren
Keren
Kim
Kint
Knudsen
Korch
Korch
Lazar Adler
Leung
Lewis
Lewis
Liew
Limmathurotsakul
Madigan
Maisonneuve
Makarova
Matthew P. Crump
Milton
Moker
Murzin
Nicholas Harmer
Porter
Richard W. Titball
Schuster
Sevillano
Shah
Singh
Studier
Subramaniam
Ulrich
Vega
Victoria A. Higman
Vranken
Wang
Wiersinga
Wiersinga
Yamaguchi
Zhao
Zhu
Publication date
7 February 2014
Publisher
'Portland Press Ltd.'
Doi
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on
PubMed
Abstract
© 2014 The Authors Journal compilation. ©2014 Biochemical Society.This is an open access article that is freely available in ORE or from the publisher's website. Please cite the published version.Published by Portland Press on behalf of the Biochemical SocietyTA (toxin-antitoxin) systems are widely distributed amongst bacteria and are associated with the formation of antibiotic tolerant (persister) cells that may have involvement in chronic and recurrent disease. We show that overexpression of the Burkholderia pseudomallei HicA toxin causes growth arrest and increases the number of persister cells tolerant to ciprofloxacin or ceftazidime. Furthermore, our data show that persistence towards ciprofloxacin or ceftazidime can be differentially modulated depending on the level of induction of HicA expression. Deleting the hicAB locus from B. pseudomallei K96243 significantly reduced persister cell frequencies following exposure to ciprofloxacin, but not ceftazidime. The structure of HicA(H24A) was solved by NMR and forms a dsRBD-like (dsRNA-binding domain-like) fold, composed of a triple-stranded β-sheet, with two helices packed against one face. The surface of the protein is highly positively charged indicative of an RNA-binding protein and His24 and Gly22 were functionality important residues. This is the first study demonstrating a role for the HicAB system in bacterial persistence and the first structure of a HicA protein that has been experimentally characterized.Wellcome Trus
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info:doi/10.1042%2Fbj20140073
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