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dc.contributor.authorde Lucas, Maria Pilar 
dc.contributor.authorJimenez, Marta 
dc.contributor.authorSanchez-Pavon, Paloma 
dc.contributor.authorSaez, Alberto G 
dc.contributor.authorLozano, Encarnacion 
dc.date.accessioned2021-02-03T10:46:54Z
dc.date.available2021-02-03T10:46:54Z
dc.date.issued2021-01-11
dc.identifier.citationInt J Mol Sci . 2021 Jan 11;22(2):638.es_ES
dc.identifier.urihttp://hdl.handle.net/20.500.12105/11786
dc.description.abstractTransforming growth factor β (TGF-β) signalling pathways are highly conserved across metazoa and play essential roles not only during development but also in adult tissue maintenance. Alterations of these pathways usually result in a plethora of pathologies. In the nematode Caenorhabditis elegans, the TGF-β Sma/Mab (small/male abnormal) pathway regulates various worm phenotypes such as body size, immune response, ageing, matricide and reproductive span. SMA-10 has been described as a positive modulator of worm body size through the TGF-β Sma/Mab pathway. To better understand if SMA-10 is a core component of the pathway, we use gene epistatic analysis to assess the contribution of SMA-10 to various phenotypes regulated by TGF-β Sma/Mab. We confirm that SMA-10 controls body size and find that it also affects the matricide and reproductive span of the nematodes. However, neither male tail formation (previously reported) nor ageing appeared altered. Lastly, although null sma-10 worms are more susceptible to Pseudomonas aeruginosa infections than wild-types, this response does not depend on TGF-β Sma/Mab but on the insulin receptor DAF-2. We also show that the expression of sma-10 in either hypodermis or intestine fully rescues the wild-type immune response. Our results contribute to understanding the role of SMA-10 as a context-dependent component of TGF-β Sma/Mab, and reveal a function of SMA-10 in immunity in association to the Insulin/insulin-like growth factor signalling (IIS) pathway.es_ES
dc.description.sponsorshipThis research was funded by Fondo de Investigaciones Sanitarias (FIS), grant numbers PI08/642 and PI11/120 to E.L., M.P.d.L., A.G.S. and E.L. were supported by programs Formación de Profesorado Universitario, FIS PI08/642 and Ramón y Cajal, respectively, all of them from the Spanish Government.es_ES
dc.language.isoenges_ES
dc.publisherMultidisciplinary Digital Publishing Institute (MDPI) es_ES
dc.type.hasVersionVoRes_ES
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/*
dc.subjectIIS pathwayes_ES
dc.subjectTGF-β Sma/Mabes_ES
dc.subjectTGF-β signallinges_ES
dc.subjectdaf-2es_ES
dc.subjectInnate immunityes_ES
dc.subjectsma-10es_ES
dc.titleSMA-10 Is a Non-Canonical Member of the TGF-β Sma/Mab Pathway and Immunity Regulator via the DAF-2 Insulin Receptor in Caenorhabditis elegans.es_ES
dc.typejournal articlees_ES
dc.rights.licenseAtribución 4.0 Internacional*
dc.identifier.pubmedID33440633es_ES
dc.format.volume22es_ES
dc.format.number2es_ES
dc.identifier.doi10.3390/ijms22020638es_ES
dc.contributor.funderInstituto de Salud Carlos III 
dc.description.peerreviewedes_ES
dc.identifier.e-issn1422-0067es_ES
dc.relation.publisherversionhttps://doi.org/10.3390/ijms22020638es_ES
dc.identifier.journalInternational journal of molecular scienceses_ES
dc.repisalud.centroISCIII::Unidad Funcional de Investigación de Enfermedades Crónicas (UFIEC)es_ES
dc.repisalud.institucionISCIIIes_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/PI08/642es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/PI11/120es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/FIS PI08/642es_ES
dc.rights.accessRightsopen accesses_ES


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Atribución 4.0 Internacional
Este Item está sujeto a una licencia Creative Commons: Atribución 4.0 Internacional