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Article: Stochastic Expression of the Interferon-beta Gene

TitleStochastic Expression of the Interferon-beta Gene
Authors
KeywordsAnimals
Cell Line
Fibroblasts/*immunology/virology
Flow Cytometry
Gene Expression Regulation
Genetic Variation
Host-Pathogen Interactions
Interferon-alpha/biosynthesis/genetics
Interferon-beta/biosynthesis/*genetics
Membrane Proteins/genetics/metabolism
Mice
Nerve Tissue Proteins/genetics/metabolism
Poly I-C/genetics
Recombinant Fusion Proteins/genetics/immunology
Sendai virus/growth & development/*immunology
Signal Transduction
Stochastic Processes
Transcription Factors/genetics/immunology
Transcription, Genetic
Virus Replication
Issue Date2012
PublisherPublic Library of Science. The Journal's web site is located at http://www.plosbiology.org/plosonline/?request=index-html
Citation
PLoS Biology, 2012, v. 10 n. 1, p. article no. e1001249 How to Cite?
AbstractVirus infection of mammalian cells induces the production of high levels of type I interferons (IFNalpha and beta), cytokines that orchestrate antiviral innate and adaptive immunity. Previous studies have shown that only a fraction of the infected cells produce IFN. However, the mechanisms responsible for this stochastic expression are poorly understood. Here we report an in depth analysis of IFN-expressing and non-expressing mouse cells infected with Sendai virus. Mouse embryonic fibroblasts in which an internal ribosome entry site/yellow fluorescent protein gene was inserted downstream from the endogenous IFNbeta gene were used to distinguish between the two cell types, and they were isolated from each other using fluorescence-activated cell sorting methods. Analysis of the separated cells revealed that stochastic IFNbeta expression is a consequence of cell-to-cell variability in the levels and/or activities of limiting components at every level of the virus induction process, ranging from viral replication and expression, to the sensing of viral RNA by host factors, to activation of the signaling pathway, to the levels of activated transcription factors. We propose that this highly complex stochastic IFNbeta gene expression evolved to optimize both the level and distribution of type I IFNs in response to virus infection.
Persistent Identifierhttp://hdl.handle.net/10722/219914
ISSN
2010 Impact Factor: 12.472
2015 SCImago Journal Rankings: 5.293
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorZhao, M-
dc.contributor.authorZhang, J-
dc.contributor.authorPhatnan, H-
dc.contributor.authorScheu, S-
dc.contributor.authorManiatis, T-
dc.date.accessioned2015-10-02T04:41:05Z-
dc.date.available2015-10-02T04:41:05Z-
dc.date.issued2012-
dc.identifier.citationPLoS Biology, 2012, v. 10 n. 1, p. article no. e1001249-
dc.identifier.issn1544-9173-
dc.identifier.urihttp://hdl.handle.net/10722/219914-
dc.description.abstractVirus infection of mammalian cells induces the production of high levels of type I interferons (IFNalpha and beta), cytokines that orchestrate antiviral innate and adaptive immunity. Previous studies have shown that only a fraction of the infected cells produce IFN. However, the mechanisms responsible for this stochastic expression are poorly understood. Here we report an in depth analysis of IFN-expressing and non-expressing mouse cells infected with Sendai virus. Mouse embryonic fibroblasts in which an internal ribosome entry site/yellow fluorescent protein gene was inserted downstream from the endogenous IFNbeta gene were used to distinguish between the two cell types, and they were isolated from each other using fluorescence-activated cell sorting methods. Analysis of the separated cells revealed that stochastic IFNbeta expression is a consequence of cell-to-cell variability in the levels and/or activities of limiting components at every level of the virus induction process, ranging from viral replication and expression, to the sensing of viral RNA by host factors, to activation of the signaling pathway, to the levels of activated transcription factors. We propose that this highly complex stochastic IFNbeta gene expression evolved to optimize both the level and distribution of type I IFNs in response to virus infection.-
dc.languageeng-
dc.publisherPublic Library of Science. The Journal's web site is located at http://www.plosbiology.org/plosonline/?request=index-html-
dc.relation.ispartofPLoS Biology-
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subjectAnimals-
dc.subjectCell Line-
dc.subjectFibroblasts/*immunology/virology-
dc.subjectFlow Cytometry-
dc.subjectGene Expression Regulation-
dc.subjectGenetic Variation-
dc.subjectHost-Pathogen Interactions-
dc.subjectInterferon-alpha/biosynthesis/genetics-
dc.subjectInterferon-beta/biosynthesis/*genetics-
dc.subjectMembrane Proteins/genetics/metabolism-
dc.subjectMice-
dc.subjectNerve Tissue Proteins/genetics/metabolism-
dc.subjectPoly I-C/genetics-
dc.subjectRecombinant Fusion Proteins/genetics/immunology-
dc.subjectSendai virus/growth & development/*immunology-
dc.subjectSignal Transduction-
dc.subjectStochastic Processes-
dc.subjectTranscription Factors/genetics/immunology-
dc.subjectTranscription, Genetic-
dc.subjectVirus Replication-
dc.titleStochastic Expression of the Interferon-beta Gene-
dc.typeArticle-
dc.identifier.emailZhang, J: jzhang1@hku.hk-
dc.identifier.authorityZhang, J=rp01713-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1371/journal.pbio.1001249-
dc.identifier.pmid22291574-
dc.identifier.pmcidPMC3265471-
dc.identifier.scopuseid_2-s2.0-84856480470-
dc.identifier.volume10-
dc.identifier.issue1-
dc.identifier.spagearticle no. e1001249-
dc.identifier.epagearticle no. e1001249-
dc.identifier.isiWOS:000300420400018-
dc.publisher.placeUnited States-

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