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dc.creatorNataf, Sergees
dc.creatorUriagereka, Juanes
dc.creatorBenítez Burraco, Antonioes
dc.date.accessioned2019-09-19T07:17:47Z
dc.date.available2019-09-19T07:17:47Z
dc.date.issued2019-04-12
dc.identifier.citationNataf, S., Uriagereka, J. y Benítez Burraco, A. (2019). The promoter regions of intellectual disability-associated genes are uniquely enriched in LTR sequences of the MEr41 primate-specific endogenous retrovirus: An evolutionary connection between immunity and cognition. Frontiers in Genetics, 10, 321-1-321-13.
dc.identifier.issn1664-8021es
dc.identifier.urihttps://hdl.handle.net/11441/89197
dc.descriptionThe Supplementary Material for this article can be found online at: https://www.frontiersin.org/articles/10.3389/fgene.2019.00321/full#supplementary-materiales
dc.description.abstractSocial behavior and neuronal connectivity in rodents have been shown to be shaped by the prototypical T lymphocyte-derived pro-inflammatory cytokine Interferon-gamma (IFNγ). It has also been demonstrated that STAT1 (Signal Transducer And Activator Of Transcription 1), a transcription factor (TF) crucially involved in the IFNγ pathway, binds consensus sequences that, in humans, are located with a high frequency in the LTRs (Long Terminal Repeats) of the MER41 family of primate-specific HERVs (Human Endogenous Retroviruses). However, the putative role of an IFNγ/STAT1/MER41 pathway in human cognition and/or behavior is still poorly documented. Here, we present evidence that the promoter regions of intellectual disability-associated genes are uniquely enriched in LTR sequences of the MER41 HERVs. This observation is specific to MER41 among more than 130 HERVs examined. Moreover, we have not found such a significant enrichment in the promoter regions of genes that associate with autism spectrum disorder (ASD) or schizophrenia. Interestingly, ID-associated genes exhibit promoter-localized MER41 LTRs that harbor TF binding sites (TFBSs) for not only STAT1 but also other immune TFs such as, in particular, NFKB1 (Nuclear Factor Kappa B Subunit 1) and STAT3 (Signal Transducer And Activator Of Transcription 3). Moreover, IL-6 (Interleukin 6) rather than IFNγ, is identified as the main candidate cytokine regulating such an immune/MER41/cognition pathway. Of note, differences between humans and chimpanzees are observed regarding the insertion sites of MER41 LTRs in the promoter regions of ID-associated genes. Finally, a survey of the human proteome has allowed us to map a protein-protein network which links the identified immune/MER41/cognition pathway to FOXP2 (Forkhead Box P2), a key TF involved in the emergence of human speech. Our work suggests that together with the evolution of immune genes, the stepped self-domestication of MER41 in the genomes of primates could have contributed to cognitive evolution. We further propose that non-inherited forms of ID might result from the untimely or quantitatively inappropriate expression of immune signals, notably IL-6, that putatively regulate cognition-associated genes via promoter-localized MER41 LTRs.es
dc.formatapplication/pdfes
dc.language.isoenges
dc.publisherFrontiers Research Foundationes
dc.relation.ispartofFrontiers in Genetics, 10, 321-1-321-13.
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 Internacional*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.subjectIntellectual disabilityes
dc.subjectCognitiones
dc.subjectInnate immunityes
dc.subjectEvolutiones
dc.subjectHERVes
dc.titleThe promoter regions of intellectual disability-associated genes are uniquely enriched in LTR sequences of the MEr41 primate-specific endogenous retrovirus: An evolutionary connection between immunity and cognitiones
dc.typeinfo:eu-repo/semantics/articlees
dcterms.identifierhttps://ror.org/03yxnpp24
dc.type.versioninfo:eu-repo/semantics/publishedVersiones
dc.rights.accessRightsinfo:eu-repo/semantics/openAccesses
dc.contributor.affiliationUniversidad de Sevilla. Departamento de Lengua Española, Lingüística y Teoría de la Literaturaes
dc.relation.publisherversionhttps://doi.org/10.3389/fgene.2019.00321es
dc.identifier.doi10.3389/fgene.2019.00321es
idus.format.extent13 p.es
dc.journaltitleFrontiers in Geneticses
dc.publication.volumen10es
dc.publication.initialPage321-1es
dc.publication.endPage321-13es

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