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Endoplasmic reticulum membranes are continuously required to maintain mitotic spindle size and forces

dc.contributor.authorAraújo, Margarida
dc.contributor.authorTavares, Alexandra
dc.contributor.authorVieira, Diana V.
dc.contributor.authorTelley, Ivo A.
dc.contributor.authorOliveira, Raquel A.
dc.date.accessioned2022-12-07T09:22:15Z
dc.date.available2022-12-07T09:22:15Z
dc.date.issued2023-01-01
dc.description.abstractMembrane organelle function, localization, and proper partitioning upon cell division depend on interactions with the cytoskeleton. Whether membrane organelles also impact the function of cytoskeletal elements remains less clear. Here, we show that acute disruption of the ER around spindle poles affects mitotic spindle size and function in Drosophila syncytial embryos. Acute ER disruption was achieved through the inhibition of ER membrane fusion by the dominant-negative cytoplasmic domain of atlastin. We reveal that when centrosome-proximal ER membranes are disrupted, specifically at metaphase, mitotic spindles become smaller, despite no significant changes in microtubule dynamics. These smaller spindles are still able to mediate sister chromatid separation, yet with decreased velocity. Furthermore, by inducing mitotic exit, we found that nuclear separation and distribution are affected by ER disruption. Our results suggest that ER integrity around spindle poles is crucial for the maintenance of mitotic spindle shape and pulling forces. In addition, ER integrity also ensures nuclear spacing during syncytial divisions.pt_PT
dc.description.versioninfo:eu-repo/semantics/publishedVersionpt_PT
dc.identifier.doi10.26508/lsa.202201540pt_PT
dc.identifier.eid85141996496
dc.identifier.issn2575-1077
dc.identifier.pmcPMC9671068
dc.identifier.pmid36379670
dc.identifier.urihttp://hdl.handle.net/10400.14/39489
dc.identifier.wos000898376200001
dc.language.isoengpt_PT
dc.peerreviewedyespt_PT
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/pt_PT
dc.titleEndoplasmic reticulum membranes are continuously required to maintain mitotic spindle size and forcespt_PT
dc.typejournal article
dspace.entity.typePublication
oaire.citation.issue1pt_PT
oaire.citation.titleLife Science Alliancept_PT
oaire.citation.volume6pt_PT
rcaap.rightsopenAccesspt_PT
rcaap.typearticlept_PT

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