Senescence is a developmental mechanism that contributes to embryonic growth and patterning
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- dc.contributor.author Storer, Mekayla, 1981-ca
- dc.contributor.author Mas Malavila, Albaca
- dc.contributor.author Robert Moreno, Alexandreca
- dc.contributor.author Pecoraro, Matteo, 1984-ca
- dc.contributor.author Ortells Campos, Mª Carmen, 1984-ca
- dc.contributor.author Giacomo, Valeria dica
- dc.contributor.author Yosef, Reutca
- dc.contributor.author Pilpel, Noamca
- dc.contributor.author Krizhanovsky, Valeryca
- dc.contributor.author Sharpe, Jamesca
- dc.contributor.author Keyes, William M., 1973-ca
- dc.date.accessioned 2015-04-30T07:24:00Z
- dc.date.available 2015-04-30T07:24:00Z
- dc.date.issued 2013ca
- dc.description.abstract Senescence is a form of cell-cycle arrest linked to tumor suppression and aging. However, it remains controversial and has not been documented in nonpathologic states. Here we describe senescence as a normal developmental mechanism found throughout the embryo, including the apical ectodermal ridge (AER) and the neural roof plate, two signaling centers in embryonic patterning. Embryonic senescent cells are nonproliferative and share features with oncogene-induced senescence (OIS), including expression of p21, p15, and mediators of the senescence-associated secretory phenotype (SASP). Interestingly, mice deficient in p21 have defects in embryonic senescence, AER maintenance, and patterning. Surprisingly, the underlying mesenchyme was identified as a source for senescence instruction in the AER, whereas the ultimate fate of these senescent cells is apoptosis and macrophage-mediated clearance. We propose that senescence is a normal programmed mechanism that plays instructive roles in development, and that OIS is an evolutionarily adapted reactivation of a developmental process.
- dc.description.sponsorship M.S. and V.D.G. are funded by ‘‘La Caixa’’ fellowships, and M.P. by an FPI fellowship from the Spanish Ministry. This work was funded in part by a Plan Nacional grant to W.M.K. from the Spanish Ministry for Science and Innovation (SAF2010-18829) and CRG core funding
- dc.format.mimetype application/pdfca
- dc.identifier.citation Storer M, Mas A, Robert-Moreno A, Pecoraro M, Ortells MC, Di Giacomo V et al. Senescence is a developmental mechanism that contributes to embryonic growth and patterning. Cell. 2013 Nov 21;155(5):1119-30. DOI: 10.1016/j.cell.2013.10.041ca
- dc.identifier.doi http://dx.doi.org/10.1016/j.cell.2013.10.041
- dc.identifier.issn 0092-8674ca
- dc.identifier.uri http://hdl.handle.net/10230/23507
- dc.language.iso engca
- dc.publisher Elsevierca
- dc.relation.ispartof Cell. 2013 Nov 21;155(5):1119-30
- dc.relation.projectID info:eu-repo/grantAgreement/ES/3PN/SAF2010-18829
- dc.rights © Elsevier This is the published version of an article http://dx.doi.org/10.1016/j.cell.2013.10.041 that appeared in the journal Cell. It is published in an Open Archive under an Elsevier user license. Details of this licence are available here: http://www.elsevier.com/about/open-access/open-access-policies/oa-license-policy/elsevier-user-licenseca
- dc.rights.accessRights info:eu-repo/semantics/openAccessca
- dc.subject.other Cèl·lules -- Envelliment
- dc.subject.other Embriologia
- dc.title Senescence is a developmental mechanism that contributes to embryonic growth and patterningca
- dc.type info:eu-repo/semantics/articleca
- dc.type.version info:eu-repo/semantics/publishedVersionca