Citation

BibTex format

@article{McCarthy:2017:10.1038/nmicrobiol.2017.27,
author = {McCarthy, RR and Mazon-Moya, MJ and Moscoso, JA and Hao, Y and Lam, JS and Bordi, C and Mostowy, S and Filloux, A},
doi = {10.1038/nmicrobiol.2017.27},
journal = {Nature Microbiology},
title = {Cyclic-di-GMP regulates lipopolysaccharide modification and contributes to Pseudomonas aeruginosa immune evasion},
url = {http://dx.doi.org/10.1038/nmicrobiol.2017.27},
volume = {2},
year = {2017}
}

RIS format (EndNote, RefMan)

TY  - JOUR
AB - Pseudomonas aeruginosa is a Gram-negative bacterial pathogen associated with acute and chronic infections. The universal cyclic-di-GMP second messenger is instrumental in the switch from a motile lifestyle to resilient biofilm as in the cystic fibrosis lung. The SadC diguanylate cyclase is associated with this patho-adaptive transition. Here, we identify an unrecognized SadC partner, WarA, which we show is a methyltransferase in complex with a putative kinase, WarB. We established that WarA binds to cyclic-di-GMP, which potentiates its methyltransferase activity. Together, WarA and WarB have structural similarities with the bifunctional Escherichia coli lipopolysaccharide (LPS) O antigen regulator WbdD. Strikingly, WarA influences P. aeruginosa O antigen modal distribution and interacts with the LPS biogenesis machinery. LPS is known to modulate the immune response in the host, and by using a zebrafish infection model, we implicate WarA in the ability of P. aeruginosa to evade detection by the host.
AU - McCarthy,RR
AU - Mazon-Moya,MJ
AU - Moscoso,JA
AU - Hao,Y
AU - Lam,JS
AU - Bordi,C
AU - Mostowy,S
AU - Filloux,A
DO - 10.1038/nmicrobiol.2017.27
PY - 2017///
SN - 2058-5276
TI - Cyclic-di-GMP regulates lipopolysaccharide modification and contributes to Pseudomonas aeruginosa immune evasion
T2 - Nature Microbiology
UR - http://dx.doi.org/10.1038/nmicrobiol.2017.27
UR - http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000406000900001&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=1ba7043ffcc86c417c072aa74d649202
UR - http://hdl.handle.net/10044/1/65679
VL - 2
ER -