Divergent evolution of the activity and regulation of the glutamate decarboxylase systems in Listeria monocytogenes EGD-e and 10403S: roles in virulence and acid tolerance

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dc.contributor.author Feehily, Conor
dc.contributor.author Finnerty, Aiden
dc.contributor.author Casey, Pat G.
dc.contributor.author Hill, Colin
dc.contributor.author Gahan, Cormac G. en
dc.contributor.author O'Byrne, Conor P.
dc.contributor.author Karatzas, Kimon-Andreas G.
dc.date.accessioned 2016-02-17T11:43:38Z
dc.date.available 2016-02-17T11:43:38Z
dc.date.issued 2014
dc.identifier.citation Feehily C, Finnerty A, Casey PG, Hill C, Gahan CGM, O’Byrne CP, et al. (2014) Divergent Evolution of the Activity and Regulation of the Glutamate Decarboxylase Systems in Listeria monocytogenes EGD-e and 10403S: Roles in Virulence and Acid Tolerance. PLoS ONE 9(11): e112649. doi:10.1371/journal.pone.0112649
dc.identifier.volume 9 en
dc.identifier.issued 11 en
dc.identifier.issn 1932-6203
dc.identifier.uri http://hdl.handle.net/10468/2321
dc.identifier.doi 10.1371/journal.pone.0112649
dc.description.abstract The glutamate decarboxylase (GAD) system has been shown to be important for the survival of Listeria monocytogenes in low pH environments. The bacterium can use this faculty to maintain pH homeostasis under acidic conditions. The accepted model for the GAD system proposes that the antiport of glutamate into the bacterial cell in exchange for c-aminobutyric acid (GABA) is coupled to an intracellular decarboxylation reaction of glutamate into GABA that consumes protons and therefore facilitates pH homeostasis. Most strains of L. monocytogenes possess three decarboxylase genes (gadD1, D2 & D3) and two antiporter genes (gadT1 & gadT2). Here, we confirm that the gadD3 encodes a glutamate decarboxylase dedicated to the intracellular GAD system (GAD(i)), which produces GABA from cytoplasmic glutamate in the absence of antiport activity. We also compare the functionality of the GAD system between two commonly studied reference strains, EGD-e and 10403S with differences in terms of acid resistance. Through functional genomics we show that EGD-e is unable to export GABA and relies exclusively in the GADi system, which is driven primarily by GadD3 in this strain. In contrast 10403S relies upon GadD2 to maintain both an intracellular and extracellular GAD system (GAD(i)/GAD(e)). Through experiments with a murinised variant of EGD-e (EGDm) in mice, we found that the GAD system plays a significant role in the overall virulence of this strain. Double mutants lacking either gadD1D3 or gadD2D3 of the GAD system displayed reduced acid tolerance and were significantly affected in their ability to cause infection following oral inoculation. Since EGDm exploits GAD(i) but not GAD(e) the results indicate that the GAD(i) system makes a contribution to virulence within the mouse. Furthermore, we also provide evidence that there might be a separate line of evolution in the GAD system between two commonly used reference strains. en
dc.description.sponsorship Science Foundation Ireland (Starting Investigator Research Grant 09/SIRG/B1570; SFI/12/RC/2273; 12/RC/2273); European Commission (Marie Curie European Reintegration Grant 265154) en
dc.format.mimetype application/pdf en
dc.language.iso en en
dc.publisher Public Library of Science en
dc.rights © 2015 Feehily et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited en
dc.rights.uri http://creativecommons.org/licenses/by/4.0/ en
dc.subject Oral infection en
dc.subject Resistance en
dc.subject Ph en
dc.subject Identification en
dc.subject Expression en
dc.subject Stress en
dc.subject Growth en
dc.subject Gene en
dc.subject Inhibition en
dc.subject Survival en
dc.title Divergent evolution of the activity and regulation of the glutamate decarboxylase systems in Listeria monocytogenes EGD-e and 10403S: roles in virulence and acid tolerance en
dc.type Article (peer-reviewed) en
dc.internal.authorcontactother Cormac Gahan, School of Microbiology, University College Cork, Cork, Ireland. +353-21-490-3000 Email: C.Gahan@ucc.ie en
dc.internal.availability Full text available en
dc.description.version Published Version en
dc.internal.wokid WOS:000345250400078
dc.contributor.funder Science Foundation Ireland
dc.contributor.funder European Commission
dc.contributor.funder National University of Ireland Galway
dc.description.status Peer reviewed en
dc.identifier.journaltitle PLOS ONE en
dc.internal.IRISemailaddress c.gahan@ucc.ie en
dc.identifier.articleid e112649


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© 2015 Feehily et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited Except where otherwise noted, this item's license is described as © 2015 Feehily et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited
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