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Myc is dispensable for cardiomyocyte development but rescues Mycn-deficient hearts through functional replacement and cell competition.

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dc.contributor.authorMunoz Martin, Noelia
dc.contributor.authorSierra, Rocio
dc.contributor.authorSchimmang, Thomas
dc.contributor.authorVilla del Campo, Cristina
dc.contributor.authorTorres, Miguel
dc.contributor.funderFondation Leducq
dc.contributor.funderMinisterio de Ciencia, Innovación y Universidades (España)
dc.contributor.funderInstituto de Salud Carlos III
dc.contributor.funderFundación La Caixa
dc.contributor.funderFundación ProCNIC
dc.date.accessioned2021-07-22T10:27:37Z
dc.date.available2021-07-22T10:27:37Z
dc.date.issued2019-02-01
dc.description.abstractMyc is considered an essential transcription factor for heart development, but cardiac defects have only been studied in global Myc loss-of-function models. Here, we eliminated Myc by recombining a Myc floxed allele with the Nkx2.5Cre driver. We observed no anatomical, cellular or functional alterations in either fetuses or adult cardiac Myc-deficient mice. We re-examined Myc expression during development and found no expression in developing cardiomyocytes. In contrast, we confirmed that Mycn is essential for cardiomyocyte proliferation and cardiogenesis. Mosaic Myc overexpression in a Mycn-deficient background shows that Myc can replace Mycn function, recovering heart development. We further show that this recovery involves the elimination of Mycn-deficient cells by cell competition. Our results indicate that Myc is dispensable in cardiomyocytes both during cardiogenesis and for adult heart homeostasis, and that Mycn is exclusively responsible for cardiomyocyte proliferation during heart development. Nonetheless, our results show that Myc can functionally replace Mycn We also show that cardiomyocytes compete according to their combined Myc and Mycn levels and that cell competition eliminates flawed cardiomyocytes, suggesting its relevance as a quality control mechanism in cardiac development.es_ES
dc.description.peerreviewedSíes_ES
dc.description.sponsorshipThis work is supported by a grant from the Fondation Leducq ['Redox Regulation of Cardiomyocyte Renewal' 17CVD04] and by grants from the Ministerio de Ciencia, Innovacion y Universidades [BFU2015-71519-P and RD16/0011/0019 (ISCIII)]. N.M.-M. was supported by a pre-doctoral contract from "la Caixa" Foundation [LACAIXA-SO14]. The CNIC is supported by the Ministerio de Ciencia, Innovacion y Universidades and the Pro CNIC Foundation, and is a Severo Ochoa Center of Excellence (SEV-2015-0505).es_ES
dc.format.number3es_ES
dc.format.page170753es_ES
dc.format.volume146es_ES
dc.identifier.citationDevelopment. 2019; 146(3):170753es_ES
dc.identifier.doi10.1242/dev.170753es_ES
dc.identifier.e-issn1477-9129es_ES
dc.identifier.issn0950-1991es_ES
dc.identifier.journalDevelopment (Cambridge, England)es_ES
dc.identifier.pubmedID30642836es_ES
dc.identifier.urihttp://hdl.handle.net/20.500.12105/13252
dc.language.isoenges_ES
dc.publisherThe Company of Biologistses_ES
dc.relation.projectFECYTinfo:eu-repo/grantAgreement/ES/BFU2015-71519-Pes_ES
dc.relation.projectFECYTinfo:eu-repo/grantAgreement/ES/RD16/0011/0019es_ES
dc.relation.projectFECYTinfo:eu-repo/grantAgreement/ES/LACAIXA-SO14es_ES
dc.relation.projectFECYTinfo:eu-repo/grantAgreement/ES/SEV-2015-0505es_ES
dc.relation.publisherversionhttps://doi.org/10.1242/dev.170753es_ES
dc.repisalud.institucionCNICes_ES
dc.repisalud.orgCNICCNIC::Grupos de investigación::Control Genético del Desarrollo y Regeneración de Órganoses_ES
dc.rights.accessRightsopen accesses_ES
dc.subject.meshCell Proliferationes_ES
dc.subject.meshOrganogenesises_ES
dc.subject.meshAnimalses_ES
dc.subject.meshFemalees_ES
dc.subject.meshHeartes_ES
dc.subject.meshMicees_ES
dc.subject.meshMice, Transgenices_ES
dc.subject.meshMyocytes, Cardiaces_ES
dc.subject.meshN-Myc Proto-Oncogene Proteines_ES
dc.subject.meshProto-Oncogene Proteins c-myces_ES
dc.titleMyc is dispensable for cardiomyocyte development but rescues Mycn-deficient hearts through functional replacement and cell competition.es_ES
dc.typejournal articlees_ES
dc.type.hasVersionVoRes_ES
dspace.entity.typePublication
relation.isAuthorOfPublication27a779c5-13e6-4979-a790-6e4585678930
relation.isAuthorOfPublication22b4ccf0-d081-489b-b7fd-735ca693a445
relation.isAuthorOfPublicationd27890c6-5721-4832-a07c-6536c38ae44f
relation.isAuthorOfPublication6ec1130e-9194-41d3-b53f-eba5fc1af5c9
relation.isAuthorOfPublication.latestForDiscovery27a779c5-13e6-4979-a790-6e4585678930
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