Glutathione activates virulence gene expression of an intracellular pathogen

Intracellular pathogens are responsible for much of the world-wide morbidity and mortality due to infectious diseases. To colonize their hosts successfully, pathogens must sense their environment and regulate virulence gene expression appropriately. Accordingly, on entry into mammalian cells, the fa...
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Autor*in:	Michelle L Reniere [verfasserIn] Aaron T Whiteley Keri L Hamilton Sonya M John Peter Lauer Richard G Brennan Daniel A Portnoy

Format:	Artikel
Sprache:	Englisch

Erschienen:	2015

Rechteinformationen:	Nutzungsrecht: © 2015 Macmillan Publishers Limited. All rights reserved 2015

Schlagwörter:	Gene expression Deoxyribonucleic acid--DNA Proteins Pathogens Mutation Bacteriology Infections Intracellular Space - metabolism Suppression, Genetic - genetics Intracellular Space - microbiology DNA - metabolism Glutathione - pharmacology Selection, Genetic - genetics Virulence - genetics Gene Expression Regulation, Bacterial - genetics Macrophages - metabolism Bacterial Proteins - metabolism Intracellular Space - drug effects Glutathione - metabolism Mutation - genetics Allosteric Regulation - drug effects Listeria monocytogenes - drug effects Listeria monocytogenes - genetics Gene Expression Regulation, Bacterial - drug effects Peptide Termination Factors - metabolism Listeria monocytogenes - pathogenicity

Übergeordnetes Werk:	Enthalten in: Nature - London : Macmillan Publishers Limited, part of Springer Nature, 1869, 517(2015), 7533, Seite 170-173
Übergeordnetes Werk:	volume:517 ; year:2015 ; number:7533 ; pages:170-173

Links:	Volltext Link aufrufen Link aufrufen Link aufrufen

DOI / URN:	10.1038/nature14029

Katalog-ID:	OLC1962480739

Internformat


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245	1	0	\|a Glutathione activates virulence gene expression of an intracellular pathogen
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520			\|a Intracellular pathogens are responsible for much of the world-wide morbidity and mortality due to infectious diseases. To colonize their hosts successfully, pathogens must sense their environment and regulate virulence gene expression appropriately. Accordingly, on entry into mammalian cells, the facultative intracellular bacterial pathogen Listeria monocytogenes remodels its transcriptional program by activating the master virulence regulator PrfA. Here we show that bacterial and host-derived glutathione are required to activate PrfA. In this study a genetic selection led to the identification of a bacterial mutant in glutathione synthase that exhibited reduced virulence gene expression and was attenuated 150-fold in mice. Genome sequencing of suppressor mutants that arose spontaneously in vivo revealed a single nucleotide change in prfA that locks the protein in the active conformation (PrfA*) and completely bypassed the requirement for glutathione during infection. Biochemical and genetic studies support a model in which glutathione-dependent PrfA activation is mediated by allosteric binding of glutathione to PrfA. Whereas glutathione and other low-molecular-weight thiols have important roles in redox homeostasis in all forms of life, here we demonstrate that glutathione represents a critical signalling molecule that activates the virulence of an intracellular pathogen.
540			\|a Nutzungsrecht: © 2015 Macmillan Publishers Limited. All rights reserved 2015
650		4	\|a Gene expression
650		4	\|a Deoxyribonucleic acid--DNA
650		4	\|a Proteins
650		4	\|a Pathogens
650		4	\|a Mutation
650		4	\|a Bacteriology
650		4	\|a Infections
650		4	\|a Intracellular Space - metabolism
650		4	\|a Suppression, Genetic - genetics
650		4	\|a Intracellular Space - microbiology
650		4	\|a DNA - metabolism
650		4	\|a Glutathione - pharmacology
650		4	\|a Selection, Genetic - genetics
650		4	\|a Virulence - genetics
650		4	\|a Gene Expression Regulation, Bacterial - genetics
650		4	\|a Macrophages - metabolism
650		4	\|a Bacterial Proteins - metabolism
650		4	\|a Intracellular Space - drug effects
650		4	\|a Glutathione - metabolism
650		4	\|a Mutation - genetics
650		4	\|a Allosteric Regulation - drug effects
650		4	\|a Listeria monocytogenes - drug effects
650		4	\|a Listeria monocytogenes - genetics
650		4	\|a Gene Expression Regulation, Bacterial - drug effects
650		4	\|a Peptide Termination Factors - metabolism
650		4	\|a Listeria monocytogenes - pathogenicity
700	0		\|a Aaron T Whiteley \|4 oth
700	0		\|a Keri L Hamilton \|4 oth
700	0		\|a Sonya M John \|4 oth
700	0		\|a Peter Lauer \|4 oth
700	0		\|a Richard G Brennan \|4 oth
700	0		\|a Daniel A Portnoy \|4 oth
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publishDate	2015
allfields	10.1038/nature14029 doi PQ20160617 (DE-627)OLC1962480739 (DE-599)GBVOLC1962480739 (PRQ)c2849-cac727d2a46fa392d0762444f151e533a312aaf88c0247f898da439c5ea507530 (KEY)0072945020150000517753300170glutathioneactivatesvirulencegeneexpressionofanint DE-627 ger DE-627 rakwb eng 070 500 DNB 500 AVZ BIODIV fid Michelle L Reniere verfasserin aut Glutathione activates virulence gene expression of an intracellular pathogen 2015 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier Intracellular pathogens are responsible for much of the world-wide morbidity and mortality due to infectious diseases. To colonize their hosts successfully, pathogens must sense their environment and regulate virulence gene expression appropriately. Accordingly, on entry into mammalian cells, the facultative intracellular bacterial pathogen Listeria monocytogenes remodels its transcriptional program by activating the master virulence regulator PrfA. Here we show that bacterial and host-derived glutathione are required to activate PrfA. In this study a genetic selection led to the identification of a bacterial mutant in glutathione synthase that exhibited reduced virulence gene expression and was attenuated 150-fold in mice. Genome sequencing of suppressor mutants that arose spontaneously in vivo revealed a single nucleotide change in prfA that locks the protein in the active conformation (PrfA*) and completely bypassed the requirement for glutathione during infection. Biochemical and genetic studies support a model in which glutathione-dependent PrfA activation is mediated by allosteric binding of glutathione to PrfA. Whereas glutathione and other low-molecular-weight thiols have important roles in redox homeostasis in all forms of life, here we demonstrate that glutathione represents a critical signalling molecule that activates the virulence of an intracellular pathogen. Nutzungsrecht: © 2015 Macmillan Publishers Limited. All rights reserved 2015 Gene expression Deoxyribonucleic acid--DNA Proteins Pathogens Mutation Bacteriology Infections Intracellular Space - metabolism Suppression, Genetic - genetics Intracellular Space - microbiology DNA - metabolism Glutathione - pharmacology Selection, Genetic - genetics Virulence - genetics Gene Expression Regulation, Bacterial - genetics Macrophages - metabolism Bacterial Proteins - metabolism Intracellular Space - drug effects Glutathione - metabolism Mutation - genetics Allosteric Regulation - drug effects Listeria monocytogenes - drug effects Listeria monocytogenes - genetics Gene Expression Regulation, Bacterial - drug effects Peptide Termination Factors - metabolism Listeria monocytogenes - pathogenicity Aaron T Whiteley oth Keri L Hamilton oth Sonya M John oth Peter Lauer oth Richard G Brennan oth Daniel A Portnoy oth Enthalten in Nature London : Macmillan Publishers Limited, part of Springer Nature, 1869 517(2015), 7533, Seite 170-173 (DE-627)129292834 (DE-600)120714-3 (DE-576)014473941 0028-0836 nnns volume:517 year:2015 number:7533 pages:170-173 http://dx.doi.org/10.1038/nature14029 Volltext http://www.ncbi.nlm.nih.gov/pubmed/25567281 http://search.proquest.com/docview/1645864414 http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=4305340&tool=pmcentrez&rendertype=abstract GBV_USEFLAG_A SYSFLAG_A GBV_OLC FID-BIODIV SSG-OLC-PHY SSG-OLC-CHE SSG-OLC-MAT SSG-OLC-FOR SSG-OLC-SPO SSG-OLC-PHA SSG-OLC-DE-84 SSG-OPC-FOR GBV_ILN_11 GBV_ILN_21 GBV_ILN_22 GBV_ILN_30 GBV_ILN_40 GBV_ILN_47 GBV_ILN_55 GBV_ILN_59 GBV_ILN_60 GBV_ILN_62 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_100 GBV_ILN_101 GBV_ILN_110 GBV_ILN_120 GBV_ILN_154 GBV_ILN_160 GBV_ILN_168 GBV_ILN_170 GBV_ILN_171 GBV_ILN_211 GBV_ILN_267 GBV_ILN_290 GBV_ILN_294 GBV_ILN_601 GBV_ILN_647 GBV_ILN_754 GBV_ILN_2001 GBV_ILN_2002 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2015 GBV_ILN_2016 GBV_ILN_2018 GBV_ILN_2020 GBV_ILN_2026 GBV_ILN_2095 GBV_ILN_2116 GBV_ILN_2120 GBV_ILN_2121 GBV_ILN_2173 GBV_ILN_2219 GBV_ILN_2221 GBV_ILN_2279 GBV_ILN_2286 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4046 GBV_ILN_4125 GBV_ILN_4219 GBV_ILN_4251 GBV_ILN_4277 GBV_ILN_4302 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4313 GBV_ILN_4314 GBV_ILN_4317 GBV_ILN_4320 GBV_ILN_4324 GBV_ILN_4700 AR 517 2015 7533 170-173
spelling	10.1038/nature14029 doi PQ20160617 (DE-627)OLC1962480739 (DE-599)GBVOLC1962480739 (PRQ)c2849-cac727d2a46fa392d0762444f151e533a312aaf88c0247f898da439c5ea507530 (KEY)0072945020150000517753300170glutathioneactivatesvirulencegeneexpressionofanint DE-627 ger DE-627 rakwb eng 070 500 DNB 500 AVZ BIODIV fid Michelle L Reniere verfasserin aut Glutathione activates virulence gene expression of an intracellular pathogen 2015 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier Intracellular pathogens are responsible for much of the world-wide morbidity and mortality due to infectious diseases. To colonize their hosts successfully, pathogens must sense their environment and regulate virulence gene expression appropriately. Accordingly, on entry into mammalian cells, the facultative intracellular bacterial pathogen Listeria monocytogenes remodels its transcriptional program by activating the master virulence regulator PrfA. Here we show that bacterial and host-derived glutathione are required to activate PrfA. In this study a genetic selection led to the identification of a bacterial mutant in glutathione synthase that exhibited reduced virulence gene expression and was attenuated 150-fold in mice. Genome sequencing of suppressor mutants that arose spontaneously in vivo revealed a single nucleotide change in prfA that locks the protein in the active conformation (PrfA*) and completely bypassed the requirement for glutathione during infection. Biochemical and genetic studies support a model in which glutathione-dependent PrfA activation is mediated by allosteric binding of glutathione to PrfA. Whereas glutathione and other low-molecular-weight thiols have important roles in redox homeostasis in all forms of life, here we demonstrate that glutathione represents a critical signalling molecule that activates the virulence of an intracellular pathogen. Nutzungsrecht: © 2015 Macmillan Publishers Limited. All rights reserved 2015 Gene expression Deoxyribonucleic acid--DNA Proteins Pathogens Mutation Bacteriology Infections Intracellular Space - metabolism Suppression, Genetic - genetics Intracellular Space - microbiology DNA - metabolism Glutathione - pharmacology Selection, Genetic - genetics Virulence - genetics Gene Expression Regulation, Bacterial - genetics Macrophages - metabolism Bacterial Proteins - metabolism Intracellular Space - drug effects Glutathione - metabolism Mutation - genetics Allosteric Regulation - drug effects Listeria monocytogenes - drug effects Listeria monocytogenes - genetics Gene Expression Regulation, Bacterial - drug effects Peptide Termination Factors - metabolism Listeria monocytogenes - pathogenicity Aaron T Whiteley oth Keri L Hamilton oth Sonya M John oth Peter Lauer oth Richard G Brennan oth Daniel A Portnoy oth Enthalten in Nature London : Macmillan Publishers Limited, part of Springer Nature, 1869 517(2015), 7533, Seite 170-173 (DE-627)129292834 (DE-600)120714-3 (DE-576)014473941 0028-0836 nnns volume:517 year:2015 number:7533 pages:170-173 http://dx.doi.org/10.1038/nature14029 Volltext http://www.ncbi.nlm.nih.gov/pubmed/25567281 http://search.proquest.com/docview/1645864414 http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=4305340&tool=pmcentrez&rendertype=abstract GBV_USEFLAG_A SYSFLAG_A GBV_OLC FID-BIODIV SSG-OLC-PHY SSG-OLC-CHE SSG-OLC-MAT SSG-OLC-FOR SSG-OLC-SPO SSG-OLC-PHA SSG-OLC-DE-84 SSG-OPC-FOR GBV_ILN_11 GBV_ILN_21 GBV_ILN_22 GBV_ILN_30 GBV_ILN_40 GBV_ILN_47 GBV_ILN_55 GBV_ILN_59 GBV_ILN_60 GBV_ILN_62 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_100 GBV_ILN_101 GBV_ILN_110 GBV_ILN_120 GBV_ILN_154 GBV_ILN_160 GBV_ILN_168 GBV_ILN_170 GBV_ILN_171 GBV_ILN_211 GBV_ILN_267 GBV_ILN_290 GBV_ILN_294 GBV_ILN_601 GBV_ILN_647 GBV_ILN_754 GBV_ILN_2001 GBV_ILN_2002 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2015 GBV_ILN_2016 GBV_ILN_2018 GBV_ILN_2020 GBV_ILN_2026 GBV_ILN_2095 GBV_ILN_2116 GBV_ILN_2120 GBV_ILN_2121 GBV_ILN_2173 GBV_ILN_2219 GBV_ILN_2221 GBV_ILN_2279 GBV_ILN_2286 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4046 GBV_ILN_4125 GBV_ILN_4219 GBV_ILN_4251 GBV_ILN_4277 GBV_ILN_4302 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4313 GBV_ILN_4314 GBV_ILN_4317 GBV_ILN_4320 GBV_ILN_4324 GBV_ILN_4700 AR 517 2015 7533 170-173
allfields_unstemmed	10.1038/nature14029 doi PQ20160617 (DE-627)OLC1962480739 (DE-599)GBVOLC1962480739 (PRQ)c2849-cac727d2a46fa392d0762444f151e533a312aaf88c0247f898da439c5ea507530 (KEY)0072945020150000517753300170glutathioneactivatesvirulencegeneexpressionofanint DE-627 ger DE-627 rakwb eng 070 500 DNB 500 AVZ BIODIV fid Michelle L Reniere verfasserin aut Glutathione activates virulence gene expression of an intracellular pathogen 2015 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier Intracellular pathogens are responsible for much of the world-wide morbidity and mortality due to infectious diseases. To colonize their hosts successfully, pathogens must sense their environment and regulate virulence gene expression appropriately. Accordingly, on entry into mammalian cells, the facultative intracellular bacterial pathogen Listeria monocytogenes remodels its transcriptional program by activating the master virulence regulator PrfA. Here we show that bacterial and host-derived glutathione are required to activate PrfA. In this study a genetic selection led to the identification of a bacterial mutant in glutathione synthase that exhibited reduced virulence gene expression and was attenuated 150-fold in mice. Genome sequencing of suppressor mutants that arose spontaneously in vivo revealed a single nucleotide change in prfA that locks the protein in the active conformation (PrfA*) and completely bypassed the requirement for glutathione during infection. Biochemical and genetic studies support a model in which glutathione-dependent PrfA activation is mediated by allosteric binding of glutathione to PrfA. Whereas glutathione and other low-molecular-weight thiols have important roles in redox homeostasis in all forms of life, here we demonstrate that glutathione represents a critical signalling molecule that activates the virulence of an intracellular pathogen. Nutzungsrecht: © 2015 Macmillan Publishers Limited. All rights reserved 2015 Gene expression Deoxyribonucleic acid--DNA Proteins Pathogens Mutation Bacteriology Infections Intracellular Space - metabolism Suppression, Genetic - genetics Intracellular Space - microbiology DNA - metabolism Glutathione - pharmacology Selection, Genetic - genetics Virulence - genetics Gene Expression Regulation, Bacterial - genetics Macrophages - metabolism Bacterial Proteins - metabolism Intracellular Space - drug effects Glutathione - metabolism Mutation - genetics Allosteric Regulation - drug effects Listeria monocytogenes - drug effects Listeria monocytogenes - genetics Gene Expression Regulation, Bacterial - drug effects Peptide Termination Factors - metabolism Listeria monocytogenes - pathogenicity Aaron T Whiteley oth Keri L Hamilton oth Sonya M John oth Peter Lauer oth Richard G Brennan oth Daniel A Portnoy oth Enthalten in Nature London : Macmillan Publishers Limited, part of Springer Nature, 1869 517(2015), 7533, Seite 170-173 (DE-627)129292834 (DE-600)120714-3 (DE-576)014473941 0028-0836 nnns volume:517 year:2015 number:7533 pages:170-173 http://dx.doi.org/10.1038/nature14029 Volltext http://www.ncbi.nlm.nih.gov/pubmed/25567281 http://search.proquest.com/docview/1645864414 http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=4305340&tool=pmcentrez&rendertype=abstract GBV_USEFLAG_A SYSFLAG_A GBV_OLC FID-BIODIV SSG-OLC-PHY SSG-OLC-CHE SSG-OLC-MAT SSG-OLC-FOR SSG-OLC-SPO SSG-OLC-PHA SSG-OLC-DE-84 SSG-OPC-FOR GBV_ILN_11 GBV_ILN_21 GBV_ILN_22 GBV_ILN_30 GBV_ILN_40 GBV_ILN_47 GBV_ILN_55 GBV_ILN_59 GBV_ILN_60 GBV_ILN_62 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_100 GBV_ILN_101 GBV_ILN_110 GBV_ILN_120 GBV_ILN_154 GBV_ILN_160 GBV_ILN_168 GBV_ILN_170 GBV_ILN_171 GBV_ILN_211 GBV_ILN_267 GBV_ILN_290 GBV_ILN_294 GBV_ILN_601 GBV_ILN_647 GBV_ILN_754 GBV_ILN_2001 GBV_ILN_2002 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2015 GBV_ILN_2016 GBV_ILN_2018 GBV_ILN_2020 GBV_ILN_2026 GBV_ILN_2095 GBV_ILN_2116 GBV_ILN_2120 GBV_ILN_2121 GBV_ILN_2173 GBV_ILN_2219 GBV_ILN_2221 GBV_ILN_2279 GBV_ILN_2286 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4046 GBV_ILN_4125 GBV_ILN_4219 GBV_ILN_4251 GBV_ILN_4277 GBV_ILN_4302 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4313 GBV_ILN_4314 GBV_ILN_4317 GBV_ILN_4320 GBV_ILN_4324 GBV_ILN_4700 AR 517 2015 7533 170-173
allfieldsGer	10.1038/nature14029 doi PQ20160617 (DE-627)OLC1962480739 (DE-599)GBVOLC1962480739 (PRQ)c2849-cac727d2a46fa392d0762444f151e533a312aaf88c0247f898da439c5ea507530 (KEY)0072945020150000517753300170glutathioneactivatesvirulencegeneexpressionofanint DE-627 ger DE-627 rakwb eng 070 500 DNB 500 AVZ BIODIV fid Michelle L Reniere verfasserin aut Glutathione activates virulence gene expression of an intracellular pathogen 2015 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier Intracellular pathogens are responsible for much of the world-wide morbidity and mortality due to infectious diseases. To colonize their hosts successfully, pathogens must sense their environment and regulate virulence gene expression appropriately. Accordingly, on entry into mammalian cells, the facultative intracellular bacterial pathogen Listeria monocytogenes remodels its transcriptional program by activating the master virulence regulator PrfA. Here we show that bacterial and host-derived glutathione are required to activate PrfA. In this study a genetic selection led to the identification of a bacterial mutant in glutathione synthase that exhibited reduced virulence gene expression and was attenuated 150-fold in mice. Genome sequencing of suppressor mutants that arose spontaneously in vivo revealed a single nucleotide change in prfA that locks the protein in the active conformation (PrfA*) and completely bypassed the requirement for glutathione during infection. Biochemical and genetic studies support a model in which glutathione-dependent PrfA activation is mediated by allosteric binding of glutathione to PrfA. Whereas glutathione and other low-molecular-weight thiols have important roles in redox homeostasis in all forms of life, here we demonstrate that glutathione represents a critical signalling molecule that activates the virulence of an intracellular pathogen. Nutzungsrecht: © 2015 Macmillan Publishers Limited. All rights reserved 2015 Gene expression Deoxyribonucleic acid--DNA Proteins Pathogens Mutation Bacteriology Infections Intracellular Space - metabolism Suppression, Genetic - genetics Intracellular Space - microbiology DNA - metabolism Glutathione - pharmacology Selection, Genetic - genetics Virulence - genetics Gene Expression Regulation, Bacterial - genetics Macrophages - metabolism Bacterial Proteins - metabolism Intracellular Space - drug effects Glutathione - metabolism Mutation - genetics Allosteric Regulation - drug effects Listeria monocytogenes - drug effects Listeria monocytogenes - genetics Gene Expression Regulation, Bacterial - drug effects Peptide Termination Factors - metabolism Listeria monocytogenes - pathogenicity Aaron T Whiteley oth Keri L Hamilton oth Sonya M John oth Peter Lauer oth Richard G Brennan oth Daniel A Portnoy oth Enthalten in Nature London : Macmillan Publishers Limited, part of Springer Nature, 1869 517(2015), 7533, Seite 170-173 (DE-627)129292834 (DE-600)120714-3 (DE-576)014473941 0028-0836 nnns volume:517 year:2015 number:7533 pages:170-173 http://dx.doi.org/10.1038/nature14029 Volltext http://www.ncbi.nlm.nih.gov/pubmed/25567281 http://search.proquest.com/docview/1645864414 http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=4305340&tool=pmcentrez&rendertype=abstract GBV_USEFLAG_A SYSFLAG_A GBV_OLC FID-BIODIV SSG-OLC-PHY SSG-OLC-CHE SSG-OLC-MAT SSG-OLC-FOR SSG-OLC-SPO SSG-OLC-PHA SSG-OLC-DE-84 SSG-OPC-FOR GBV_ILN_11 GBV_ILN_21 GBV_ILN_22 GBV_ILN_30 GBV_ILN_40 GBV_ILN_47 GBV_ILN_55 GBV_ILN_59 GBV_ILN_60 GBV_ILN_62 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_100 GBV_ILN_101 GBV_ILN_110 GBV_ILN_120 GBV_ILN_154 GBV_ILN_160 GBV_ILN_168 GBV_ILN_170 GBV_ILN_171 GBV_ILN_211 GBV_ILN_267 GBV_ILN_290 GBV_ILN_294 GBV_ILN_601 GBV_ILN_647 GBV_ILN_754 GBV_ILN_2001 GBV_ILN_2002 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2015 GBV_ILN_2016 GBV_ILN_2018 GBV_ILN_2020 GBV_ILN_2026 GBV_ILN_2095 GBV_ILN_2116 GBV_ILN_2120 GBV_ILN_2121 GBV_ILN_2173 GBV_ILN_2219 GBV_ILN_2221 GBV_ILN_2279 GBV_ILN_2286 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4046 GBV_ILN_4125 GBV_ILN_4219 GBV_ILN_4251 GBV_ILN_4277 GBV_ILN_4302 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4313 GBV_ILN_4314 GBV_ILN_4317 GBV_ILN_4320 GBV_ILN_4324 GBV_ILN_4700 AR 517 2015 7533 170-173
allfieldsSound	10.1038/nature14029 doi PQ20160617 (DE-627)OLC1962480739 (DE-599)GBVOLC1962480739 (PRQ)c2849-cac727d2a46fa392d0762444f151e533a312aaf88c0247f898da439c5ea507530 (KEY)0072945020150000517753300170glutathioneactivatesvirulencegeneexpressionofanint DE-627 ger DE-627 rakwb eng 070 500 DNB 500 AVZ BIODIV fid Michelle L Reniere verfasserin aut Glutathione activates virulence gene expression of an intracellular pathogen 2015 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier Intracellular pathogens are responsible for much of the world-wide morbidity and mortality due to infectious diseases. To colonize their hosts successfully, pathogens must sense their environment and regulate virulence gene expression appropriately. Accordingly, on entry into mammalian cells, the facultative intracellular bacterial pathogen Listeria monocytogenes remodels its transcriptional program by activating the master virulence regulator PrfA. Here we show that bacterial and host-derived glutathione are required to activate PrfA. In this study a genetic selection led to the identification of a bacterial mutant in glutathione synthase that exhibited reduced virulence gene expression and was attenuated 150-fold in mice. Genome sequencing of suppressor mutants that arose spontaneously in vivo revealed a single nucleotide change in prfA that locks the protein in the active conformation (PrfA*) and completely bypassed the requirement for glutathione during infection. Biochemical and genetic studies support a model in which glutathione-dependent PrfA activation is mediated by allosteric binding of glutathione to PrfA. Whereas glutathione and other low-molecular-weight thiols have important roles in redox homeostasis in all forms of life, here we demonstrate that glutathione represents a critical signalling molecule that activates the virulence of an intracellular pathogen. Nutzungsrecht: © 2015 Macmillan Publishers Limited. All rights reserved 2015 Gene expression Deoxyribonucleic acid--DNA Proteins Pathogens Mutation Bacteriology Infections Intracellular Space - metabolism Suppression, Genetic - genetics Intracellular Space - microbiology DNA - metabolism Glutathione - pharmacology Selection, Genetic - genetics Virulence - genetics Gene Expression Regulation, Bacterial - genetics Macrophages - metabolism Bacterial Proteins - metabolism Intracellular Space - drug effects Glutathione - metabolism Mutation - genetics Allosteric Regulation - drug effects Listeria monocytogenes - drug effects Listeria monocytogenes - genetics Gene Expression Regulation, Bacterial - drug effects Peptide Termination Factors - metabolism Listeria monocytogenes - pathogenicity Aaron T Whiteley oth Keri L Hamilton oth Sonya M John oth Peter Lauer oth Richard G Brennan oth Daniel A Portnoy oth Enthalten in Nature London : Macmillan Publishers Limited, part of Springer Nature, 1869 517(2015), 7533, Seite 170-173 (DE-627)129292834 (DE-600)120714-3 (DE-576)014473941 0028-0836 nnns volume:517 year:2015 number:7533 pages:170-173 http://dx.doi.org/10.1038/nature14029 Volltext http://www.ncbi.nlm.nih.gov/pubmed/25567281 http://search.proquest.com/docview/1645864414 http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=4305340&tool=pmcentrez&rendertype=abstract GBV_USEFLAG_A SYSFLAG_A GBV_OLC FID-BIODIV SSG-OLC-PHY SSG-OLC-CHE SSG-OLC-MAT SSG-OLC-FOR SSG-OLC-SPO SSG-OLC-PHA SSG-OLC-DE-84 SSG-OPC-FOR GBV_ILN_11 GBV_ILN_21 GBV_ILN_22 GBV_ILN_30 GBV_ILN_40 GBV_ILN_47 GBV_ILN_55 GBV_ILN_59 GBV_ILN_60 GBV_ILN_62 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_100 GBV_ILN_101 GBV_ILN_110 GBV_ILN_120 GBV_ILN_154 GBV_ILN_160 GBV_ILN_168 GBV_ILN_170 GBV_ILN_171 GBV_ILN_211 GBV_ILN_267 GBV_ILN_290 GBV_ILN_294 GBV_ILN_601 GBV_ILN_647 GBV_ILN_754 GBV_ILN_2001 GBV_ILN_2002 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2015 GBV_ILN_2016 GBV_ILN_2018 GBV_ILN_2020 GBV_ILN_2026 GBV_ILN_2095 GBV_ILN_2116 GBV_ILN_2120 GBV_ILN_2121 GBV_ILN_2173 GBV_ILN_2219 GBV_ILN_2221 GBV_ILN_2279 GBV_ILN_2286 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4046 GBV_ILN_4125 GBV_ILN_4219 GBV_ILN_4251 GBV_ILN_4277 GBV_ILN_4302 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4313 GBV_ILN_4314 GBV_ILN_4317 GBV_ILN_4320 GBV_ILN_4324 GBV_ILN_4700 AR 517 2015 7533 170-173
language	English
source	Enthalten in Nature 517(2015), 7533, Seite 170-173 volume:517 year:2015 number:7533 pages:170-173
sourceStr	Enthalten in Nature 517(2015), 7533, Seite 170-173 volume:517 year:2015 number:7533 pages:170-173
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Gene expression Deoxyribonucleic acid--DNA Proteins Pathogens Mutation Bacteriology Infections Intracellular Space - metabolism Suppression, Genetic - genetics Intracellular Space - microbiology DNA - metabolism Glutathione - pharmacology Selection, Genetic - genetics Virulence - genetics Gene Expression Regulation, Bacterial - genetics Macrophages - metabolism Bacterial Proteins - metabolism Intracellular Space - drug effects Glutathione - metabolism Mutation - genetics Allosteric Regulation - drug effects Listeria monocytogenes - drug effects Listeria monocytogenes - genetics Gene Expression Regulation, Bacterial - drug effects Peptide Termination Factors - metabolism Listeria monocytogenes - pathogenicity
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container_title	Nature
authorswithroles_txt_mv	Michelle L Reniere @@aut@@ Aaron T Whiteley @@oth@@ Keri L Hamilton @@oth@@ Sonya M John @@oth@@ Peter Lauer @@oth@@ Richard G Brennan @@oth@@ Daniel A Portnoy @@oth@@
publishDateDaySort_date	2015-01-01T00:00:00Z
hierarchy_top_id	129292834
dewey-sort	270
id	OLC1962480739
language_de	englisch
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author	Michelle L Reniere
spellingShingle	Michelle L Reniere ddc 070 ddc 500 fid BIODIV misc Gene expression misc Deoxyribonucleic acid--DNA misc Proteins misc Pathogens misc Mutation misc Bacteriology misc Infections misc Intracellular Space - metabolism misc Suppression, Genetic - genetics misc Intracellular Space - microbiology misc DNA - metabolism misc Glutathione - pharmacology misc Selection, Genetic - genetics misc Virulence - genetics misc Gene Expression Regulation, Bacterial - genetics misc Macrophages - metabolism misc Bacterial Proteins - metabolism misc Intracellular Space - drug effects misc Glutathione - metabolism misc Mutation - genetics misc Allosteric Regulation - drug effects misc Listeria monocytogenes - drug effects misc Listeria monocytogenes - genetics misc Gene Expression Regulation, Bacterial - drug effects misc Peptide Termination Factors - metabolism misc Listeria monocytogenes - pathogenicity Glutathione activates virulence gene expression of an intracellular pathogen
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topic_title	070 500 DNB 500 AVZ BIODIV fid Glutathione activates virulence gene expression of an intracellular pathogen Gene expression Deoxyribonucleic acid--DNA Proteins Pathogens Mutation Bacteriology Infections Intracellular Space - metabolism Suppression, Genetic - genetics Intracellular Space - microbiology DNA - metabolism Glutathione - pharmacology Selection, Genetic - genetics Virulence - genetics Gene Expression Regulation, Bacterial - genetics Macrophages - metabolism Bacterial Proteins - metabolism Intracellular Space - drug effects Glutathione - metabolism Mutation - genetics Allosteric Regulation - drug effects Listeria monocytogenes - drug effects Listeria monocytogenes - genetics Gene Expression Regulation, Bacterial - drug effects Peptide Termination Factors - metabolism Listeria monocytogenes - pathogenicity
topic	ddc 070 ddc 500 fid BIODIV misc Gene expression misc Deoxyribonucleic acid--DNA misc Proteins misc Pathogens misc Mutation misc Bacteriology misc Infections misc Intracellular Space - metabolism misc Suppression, Genetic - genetics misc Intracellular Space - microbiology misc DNA - metabolism misc Glutathione - pharmacology misc Selection, Genetic - genetics misc Virulence - genetics misc Gene Expression Regulation, Bacterial - genetics misc Macrophages - metabolism misc Bacterial Proteins - metabolism misc Intracellular Space - drug effects misc Glutathione - metabolism misc Mutation - genetics misc Allosteric Regulation - drug effects misc Listeria monocytogenes - drug effects misc Listeria monocytogenes - genetics misc Gene Expression Regulation, Bacterial - drug effects misc Peptide Termination Factors - metabolism misc Listeria monocytogenes - pathogenicity
topic_unstemmed	ddc 070 ddc 500 fid BIODIV misc Gene expression misc Deoxyribonucleic acid--DNA misc Proteins misc Pathogens misc Mutation misc Bacteriology misc Infections misc Intracellular Space - metabolism misc Suppression, Genetic - genetics misc Intracellular Space - microbiology misc DNA - metabolism misc Glutathione - pharmacology misc Selection, Genetic - genetics misc Virulence - genetics misc Gene Expression Regulation, Bacterial - genetics misc Macrophages - metabolism misc Bacterial Proteins - metabolism misc Intracellular Space - drug effects misc Glutathione - metabolism misc Mutation - genetics misc Allosteric Regulation - drug effects misc Listeria monocytogenes - drug effects misc Listeria monocytogenes - genetics misc Gene Expression Regulation, Bacterial - drug effects misc Peptide Termination Factors - metabolism misc Listeria monocytogenes - pathogenicity
topic_browse	ddc 070 ddc 500 fid BIODIV misc Gene expression misc Deoxyribonucleic acid--DNA misc Proteins misc Pathogens misc Mutation misc Bacteriology misc Infections misc Intracellular Space - metabolism misc Suppression, Genetic - genetics misc Intracellular Space - microbiology misc DNA - metabolism misc Glutathione - pharmacology misc Selection, Genetic - genetics misc Virulence - genetics misc Gene Expression Regulation, Bacterial - genetics misc Macrophages - metabolism misc Bacterial Proteins - metabolism misc Intracellular Space - drug effects misc Glutathione - metabolism misc Mutation - genetics misc Allosteric Regulation - drug effects misc Listeria monocytogenes - drug effects misc Listeria monocytogenes - genetics misc Gene Expression Regulation, Bacterial - drug effects misc Peptide Termination Factors - metabolism misc Listeria monocytogenes - pathogenicity
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title	Glutathione activates virulence gene expression of an intracellular pathogen
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title_full	Glutathione activates virulence gene expression of an intracellular pathogen
author_sort	Michelle L Reniere
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title_sort	glutathione activates virulence gene expression of an intracellular pathogen
title_auth	Glutathione activates virulence gene expression of an intracellular pathogen
abstract	Intracellular pathogens are responsible for much of the world-wide morbidity and mortality due to infectious diseases. To colonize their hosts successfully, pathogens must sense their environment and regulate virulence gene expression appropriately. Accordingly, on entry into mammalian cells, the facultative intracellular bacterial pathogen Listeria monocytogenes remodels its transcriptional program by activating the master virulence regulator PrfA. Here we show that bacterial and host-derived glutathione are required to activate PrfA. In this study a genetic selection led to the identification of a bacterial mutant in glutathione synthase that exhibited reduced virulence gene expression and was attenuated 150-fold in mice. Genome sequencing of suppressor mutants that arose spontaneously in vivo revealed a single nucleotide change in prfA that locks the protein in the active conformation (PrfA*) and completely bypassed the requirement for glutathione during infection. Biochemical and genetic studies support a model in which glutathione-dependent PrfA activation is mediated by allosteric binding of glutathione to PrfA. Whereas glutathione and other low-molecular-weight thiols have important roles in redox homeostasis in all forms of life, here we demonstrate that glutathione represents a critical signalling molecule that activates the virulence of an intracellular pathogen.
abstractGer	Intracellular pathogens are responsible for much of the world-wide morbidity and mortality due to infectious diseases. To colonize their hosts successfully, pathogens must sense their environment and regulate virulence gene expression appropriately. Accordingly, on entry into mammalian cells, the facultative intracellular bacterial pathogen Listeria monocytogenes remodels its transcriptional program by activating the master virulence regulator PrfA. Here we show that bacterial and host-derived glutathione are required to activate PrfA. In this study a genetic selection led to the identification of a bacterial mutant in glutathione synthase that exhibited reduced virulence gene expression and was attenuated 150-fold in mice. Genome sequencing of suppressor mutants that arose spontaneously in vivo revealed a single nucleotide change in prfA that locks the protein in the active conformation (PrfA*) and completely bypassed the requirement for glutathione during infection. Biochemical and genetic studies support a model in which glutathione-dependent PrfA activation is mediated by allosteric binding of glutathione to PrfA. Whereas glutathione and other low-molecular-weight thiols have important roles in redox homeostasis in all forms of life, here we demonstrate that glutathione represents a critical signalling molecule that activates the virulence of an intracellular pathogen.
abstract_unstemmed	Intracellular pathogens are responsible for much of the world-wide morbidity and mortality due to infectious diseases. To colonize their hosts successfully, pathogens must sense their environment and regulate virulence gene expression appropriately. Accordingly, on entry into mammalian cells, the facultative intracellular bacterial pathogen Listeria monocytogenes remodels its transcriptional program by activating the master virulence regulator PrfA. Here we show that bacterial and host-derived glutathione are required to activate PrfA. In this study a genetic selection led to the identification of a bacterial mutant in glutathione synthase that exhibited reduced virulence gene expression and was attenuated 150-fold in mice. Genome sequencing of suppressor mutants that arose spontaneously in vivo revealed a single nucleotide change in prfA that locks the protein in the active conformation (PrfA*) and completely bypassed the requirement for glutathione during infection. Biochemical and genetic studies support a model in which glutathione-dependent PrfA activation is mediated by allosteric binding of glutathione to PrfA. Whereas glutathione and other low-molecular-weight thiols have important roles in redox homeostasis in all forms of life, here we demonstrate that glutathione represents a critical signalling molecule that activates the virulence of an intracellular pathogen.
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title_short	Glutathione activates virulence gene expression of an intracellular pathogen
url	http://dx.doi.org/10.1038/nature14029 http://www.ncbi.nlm.nih.gov/pubmed/25567281 http://search.proquest.com/docview/1645864414 http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=4305340&tool=pmcentrez&rendertype=abstract
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up_date	2024-07-04T03:41:17.416Z
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fullrecord_marcxml	<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a2200265 4500</leader><controlfield tag="001">OLC1962480739</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230714155607.0</controlfield><controlfield tag="007">tu</controlfield><controlfield tag="008">160206s2015 xx \|\|\|\|\| 00\| \|\|eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1038/nature14029</subfield><subfield code="2">doi</subfield></datafield><datafield tag="028" ind1="5" ind2="2"><subfield code="a">PQ20160617</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)OLC1962480739</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-599)GBVOLC1962480739</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(PRQ)c2849-cac727d2a46fa392d0762444f151e533a312aaf88c0247f898da439c5ea507530</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(KEY)0072945020150000517753300170glutathioneactivatesvirulencegeneexpressionofanint</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">070</subfield><subfield code="a">500</subfield><subfield code="q">DNB</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">500</subfield><subfield code="q">AVZ</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">BIODIV</subfield><subfield code="2">fid</subfield></datafield><datafield tag="100" ind1="0" ind2=" "><subfield code="a">Michelle L Reniere</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Glutathione activates virulence gene expression of an intracellular pathogen</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2015</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">ohne Hilfsmittel zu benutzen</subfield><subfield code="b">n</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Band</subfield><subfield code="b">nc</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Intracellular pathogens are responsible for much of the world-wide morbidity and mortality due to infectious diseases. To colonize their hosts successfully, pathogens must sense their environment and regulate virulence gene expression appropriately. Accordingly, on entry into mammalian cells, the facultative intracellular bacterial pathogen Listeria monocytogenes remodels its transcriptional program by activating the master virulence regulator PrfA. Here we show that bacterial and host-derived glutathione are required to activate PrfA. In this study a genetic selection led to the identification of a bacterial mutant in glutathione synthase that exhibited reduced virulence gene expression and was attenuated 150-fold in mice. Genome sequencing of suppressor mutants that arose spontaneously in vivo revealed a single nucleotide change in prfA that locks the protein in the active conformation (PrfA*) and completely bypassed the requirement for glutathione during infection. Biochemical and genetic studies support a model in which glutathione-dependent PrfA activation is mediated by allosteric binding of glutathione to PrfA. Whereas glutathione and other low-molecular-weight thiols have important roles in redox homeostasis in all forms of life, here we demonstrate that glutathione represents a critical signalling molecule that activates the virulence of an intracellular pathogen.</subfield></datafield><datafield tag="540" ind1=" " ind2=" "><subfield code="a">Nutzungsrecht: © 2015 Macmillan Publishers Limited. All rights reserved 2015</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Gene expression</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Deoxyribonucleic acid--DNA</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Proteins</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Pathogens</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Mutation</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Bacteriology</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Infections</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Intracellular Space - metabolism</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Suppression, Genetic - genetics</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Intracellular 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Glutathione activates virulence gene expression of an intracellular pathogen

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