dc.contributor.author | Izquierdo-Villalba, Ismael | |
dc.contributor.author | Mirra, Serena | |
dc.contributor.author | Manso, Yasmina | |
dc.contributor.author | Parcerisas, Antoni | |
dc.contributor.author | Rubio, Javier | |
dc.contributor.author | Del Valle, Jaume | |
dc.contributor.author | Gil-Bea, Francisco J | |
dc.contributor.author | Ulloa, Fausto | |
dc.contributor.author | Herrero-Lorenzo, Marina | |
dc.contributor.author | Verdaguer, Ester | |
dc.contributor.author | Benincá, Cristiane | |
dc.contributor.author | Castro-Torres, Rubén D | |
dc.contributor.author | Rebollo, Elena | |
dc.contributor.author | Marfany, Gemma | |
dc.contributor.author | Auladell, Carme | |
dc.contributor.author | Navarro, Xavier | |
dc.contributor.author | Enriquez, Jose Antonio | |
dc.contributor.author | López de Munain, Adolfo | |
dc.contributor.author | Soriano, Eduardo | |
dc.contributor.author | Aragay, Anna M | |
dc.date.accessioned | 2024-07-09T13:19:26Z | |
dc.date.available | 2024-07-09T13:19:26Z | |
dc.date.issued | 2024-02-06 | |
dc.identifier.citation | Sci Signal. 2024 Feb 6;17(822):eabq1007. | es_ES |
dc.identifier.uri | http://hdl.handle.net/20.500.12105/20363 | |
dc.description.abstract | Mitochondrial dynamics and trafficking are essential to provide the energy required for neurotransmission and neural activity. We investigated how G protein-coupled receptors (GPCRs) and G proteins control mitochondrial dynamics and trafficking. The activation of Gαq inhibited mitochondrial trafficking in neurons through a mechanism that was independent of the canonical downstream PLCβ pathway. Mitoproteome analysis revealed that Gαq interacted with the Eutherian-specific mitochondrial protein armadillo repeat-containing X-linked protein 3 (Alex3) and the Miro1/Trak2 complex, which acts as an adaptor for motor proteins involved in mitochondrial trafficking along dendrites and axons. By generating a CNS-specific Alex3 knockout mouse line, we demonstrated that Alex3 was required for the effects of Gαq on mitochondrial trafficking and dendritic growth in neurons. Alex3-deficient mice had altered amounts of ER stress response proteins, increased neuronal death, motor neuron loss, and severe motor deficits. These data revealed a mammalian-specific Alex3/Gαq mitochondrial complex, which enables control of mitochondrial trafficking and neuronal death by GPCRs. | es_ES |
dc.description.sponsorship | This work was funded by the Ministerio de Ciencia e Innovación (grants BFU2017-
83379-R to A.M.A., SAF2016-76340R PID2019-106764RB-C21 and PID2022-138105OB-C21 to
E.S., SAF2015-65633-R and RTI2018-099357-B-I00 to J.A.E., RTI2018-096386-B-I00 to X.N.,
EQC2018-004541-P support to E.R., Severo Ochoa Excellence program to J.A.E., and María de
Maeztu Excellence program to E.S.), CSIC13-4E-2065 to the Molecular Imaging Platform, and
Instituto de Salud Carlos III (CIBERNED to E.S., C.A., X.N. and A.L.d.M.; CIBERER to G.M.; CIBERFES
to J.A.E.; grant PI18/01066 to A.L.d.M.; and a collaborative CIBERNED project to E.S. and
A.L.d.M.). J.A.E. is supported by the HFSP (RGP0016/2018) and the Pro CNIC Foundation.
A.L.d.M. is supported by EiTB Maratoia, grant number BIO17/ND/023, and by Osasun Saila,
Eusko Jaurlaritzako, grant number 2015111122. F.J.G.-B. was supported by Roche Stop Fuga de
Cerebros (BIO19/ROCHE/017/BD). I.I.-V. was supported by an FI fellowship from AGAUR | es_ES |
dc.language.iso | eng | es_ES |
dc.publisher | American Association for the Advancement of Science (AAAS) | es_ES |
dc.type.hasVersion | VoR | es_ES |
dc.rights.uri | http://creativecommons.org/licenses/by/4.0/ | * |
dc.subject.mesh | Axons | es_ES |
dc.subject.mesh | Neurons | es_ES |
dc.subject.mesh | Animals | es_ES |
dc.subject.mesh | Mice | es_ES |
dc.subject.mesh | Mammals | es_ES |
dc.subject.mesh | Mitochondrial Proteins | es_ES |
dc.title | A mammalian-specific Alex3/Gαq protein complex regulates mitochondrial trafficking, dendritic complexity, and neuronal survival. | es_ES |
dc.type | journal article | es_ES |
dc.rights.license | Atribución 4.0 Internacional | * |
dc.identifier.pubmedID | 38320000 | es_ES |
dc.format.volume | 17 | es_ES |
dc.format.number | 822 | es_ES |
dc.format.page | eabq1007 | es_ES |
dc.identifier.doi | 10.1126/scisignal.abq1007 | es_ES |
dc.contributor.funder | Ministerio de Ciencia e Innovación (España) | es_ES |
dc.contributor.funder | Ministerio de Ciencia e Innovación. Centro de Excelencia Severo Ochoa (España) | es_ES |
dc.contributor.funder | Fundación ProCNIC | es_ES |
dc.description.peerreviewed | Sí | es_ES |
dc.identifier.e-issn | 1937-9145 | es_ES |
dc.relation.publisherversion | 10.1126/scisignal.abq1007 | es_ES |
dc.identifier.journal | Science signaling | es_ES |
dc.repisalud.orgCNIC | CNIC::Grupos de investigación::Genética Funcional del Sistema de Fosforilación Oxidativa | es_ES |
dc.repisalud.institucion | CNIC | es_ES |
dc.rights.accessRights | open access | es_ES |
dc.relation.projectFECYT | info:eu-repo/grantAgreement/ES/BFU2017-83379-R | es_ES |
dc.relation.projectFECYT | info:eu-repo/grantAgreement/ES/SAF2016-76340R | es_ES |
dc.relation.projectFECYT | info:eu-repo/grantAgreement/ES/PID2019-106764RBC21 | es_ES |
dc.relation.projectFECYT | info:eu-repo/grantAgreement/ES/PID2022-138105OB-C21 | es_ES |
dc.relation.projectFECYT | info:eu-repo/grantAgreement/ES/SAF2015-65633-R | es_ES |
dc.relation.projectFECYT | info:eu-repo/grantAgreement/ES/RTI2018-099357-B-I00 | es_ES |
dc.relation.projectFECYT | info:eu-repo/grantAgreement/ES/RTI2018-096386-B-I00 | es_ES |
dc.relation.projectFECYT | info:eu-repo/grantAgreement/ES/EQC2018-004541-P | es_ES |
dc.relation.projectFECYT | info:eu-repo/grantAgreement/ES/PI18/01066 | es_ES |
dc.relation.projectFECYT | info:eu-repo/grantAgreement/ES/RGP0016/2018 | es_ES |
dc.relation.projectFECYT | info:eu-repo/grantAgreement/ES/2015111122 | es_ES |