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Shielding of actin by the endoplasmic reticulum impacts nuclear positioning

2022Journal article Open access
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dc.contributor.authorJanota, Cátia
dc.contributor.authorPinto, Andreia
dc.contributor.authorPezzarossa, Anna
dc.contributor.authorMachado, Pedro
dc.contributor.authorCosta, Judite
dc.contributor.authorCampinho, Pedro
dc.contributor.authorFranco, Claudio
dc.contributor.authorGomes, Edgar
dc.date.accessioned2022-05-24T14:30:56Z
dc.date.available2022-05-24T14:30:56Z
dc.date.issued2022
dc.description© The Author(s) 2022. Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.pt_PT
dc.description.abstractNuclear position is central to cell polarization, and its disruption is associated with various pathologies. The nucleus is moved away from the leading edge of migrating cells through its connection to moving dorsal actin cables, and the absence of connections to immobile ventral stress fibers. It is unclear how these asymmetric nucleo-cytoskeleton connections are established. Here, using an in vitro wound assay, we find that remodeling of endoplasmic reticulum (ER) impacts nuclear positioning through the formation of a barrier that shields immobile ventral stress fibers. The remodeling of ER and perinuclear ER accumulation is mediated by the ER shaping protein Climp-63. Furthermore, ectopic recruitment of the ER to stress fibers restores nuclear positioning in the absence of Climp-63. Our findings suggest that the ER mediates asymmetric nucleo-cytoskeleton connections to position the nucleus.pt_PT
dc.description.sponsorshipThis work was supported by the European Research Council H2020-GA 810207-ARPCOMPLEXITY and FP7-GA 617676 PHONICS (ERG), EMBO installation (ERG), Marine Biological Laboratory Whitman Center Fellowship (ERG), Association pour la Recherche sur le Cancer and La Ligue Nacionale contre le Cancer (ERG) and Fundação para a Ciência e a Tecnologia (SFRH/BD/112286/2015)(CJ), European Research Council H2020-GA 679368 AXIAL.EC (CF); Fundação para a Ciência e Tecnologia (PTDC/MED-PAT/31639/2017; CEECIND/04251/2017)(CF) and Fondation LeDucq (17CVD03)(CF).pt_PT
dc.description.versioninfo:eu-repo/semantics/publishedVersionpt_PT
dc.identifier.citationNat Commun. 2022 May 19;13(1):2763pt_PT
dc.identifier.doi10.1038/s41467-022-30388-3pt_PT
dc.identifier.eissn2041-1723
dc.identifier.urihttp://hdl.handle.net/10451/53158
dc.language.isoengpt_PT
dc.peerreviewedyespt_PT
dc.publisherSpringer Naturept_PT
dc.relationA role for actin remodeling around the nucleus on nuclear positioning during cell migration with implications for medulloblastoma formation
dc.relationDeregulated Endothelial Blood Flow Response as a cause of Diabetic Retinopathy
dc.relationNot Available
dc.relationDefining the role of Arp2/3 complex diversity at multiple scales of biology
dc.relationPositioning the nucleus for cell migration and muscle fiber function
dc.relationPRINCIPLES OF AXIAL POLARITY-DRIVEN VASCULAR PATTERNING
dc.relation.publisherversionhttps://www.nature.com/ncomms/pt_PT
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/pt_PT
dc.titleShielding of actin by the endoplasmic reticulum impacts nuclear positioningpt_PT
dc.typejournal article
dspace.entity.typePublication
oaire.awardTitleA role for actin remodeling around the nucleus on nuclear positioning during cell migration with implications for medulloblastoma formation
oaire.awardTitleDeregulated Endothelial Blood Flow Response as a cause of Diabetic Retinopathy
oaire.awardTitleNot Available
oaire.awardTitleDefining the role of Arp2/3 complex diversity at multiple scales of biology
oaire.awardTitlePositioning the nucleus for cell migration and muscle fiber function
oaire.awardTitlePRINCIPLES OF AXIAL POLARITY-DRIVEN VASCULAR PATTERNING
oaire.awardURIinfo:eu-repo/grantAgreement/FCT//SFRH%2FBD%2F112286%2F2015/PT
oaire.awardURIinfo:eu-repo/grantAgreement/FCT/3599-PPCDT/PTDC%2FMED-PAT%2F31639%2F2017/PT
oaire.awardURIinfo:eu-repo/grantAgreement/FCT/CEEC IND 2017/CEECIND%2F04251%2F2017%2FCP1396%2FCT0010/PT
oaire.awardURIinfo:eu-repo/grantAgreement/EC/H2020/810207/EU
oaire.awardURIinfo:eu-repo/grantAgreement/EC/FP7/617676/EU
oaire.awardURIinfo:eu-repo/grantAgreement/EC/H2020/679368/EU
oaire.citation.issue1pt_PT
oaire.citation.titleNature Communicationspt_PT
oaire.citation.volume13pt_PT
oaire.fundingStream3599-PPCDT
oaire.fundingStreamCEEC IND 2017
oaire.fundingStreamH2020
oaire.fundingStreamFP7
oaire.fundingStreamH2020
person.familyNameJanota
person.familyNamePinto
person.familyNamePezzarossa
person.familyNameCosta
person.familyNameCampinho
person.familyNameFranco
person.familyNameGomes
person.givenNameCátia
person.givenNameAndreia
person.givenNameAnna
person.givenNameJudite
person.givenNamePedro
person.givenNameClaudio
person.givenNameEdgar
person.identifierD-8117-2015
person.identifier.ciencia-id441A-AF1B-0117
person.identifier.ciencia-idDF1E-A3EE-D92D
person.identifier.ciencia-idF012-B7D6-AE72
person.identifier.ciencia-id6215-9445-3042
person.identifier.orcid0000-0003-2187-2361
person.identifier.orcid0000-0002-0840-6844
person.identifier.orcid0000-0003-1637-3891
person.identifier.orcid0000-0002-0929-475X
person.identifier.orcid0000-0002-8526-5416
person.identifier.orcid0000-0002-2861-3883
person.identifier.orcid0000-0002-6941-4872
person.identifier.ridD-9000-2015
person.identifier.scopus-author-id55386267300
person.identifier.scopus-author-id24280736600
person.identifier.scopus-author-id7102464212
project.funder.identifierhttp://doi.org/10.13039/501100001871
project.funder.identifierhttp://doi.org/10.13039/501100001871
project.funder.identifierhttp://doi.org/10.13039/501100001871
project.funder.identifierhttp://doi.org/10.13039/501100008530
project.funder.identifierhttp://doi.org/10.13039/501100008530
project.funder.identifierhttp://doi.org/10.13039/501100008530
project.funder.nameFundação para a Ciência e a Tecnologia
project.funder.nameFundação para a Ciência e a Tecnologia
project.funder.nameFundação para a Ciência e a Tecnologia
project.funder.nameEuropean Commission
project.funder.nameEuropean Commission
project.funder.nameEuropean Commission
rcaap.rightsopenAccesspt_PT
rcaap.typearticlept_PT
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