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dc.contributor.authorBossing, T
dc.contributor.authorBarros, CS
dc.contributor.authorFischer, B
dc.contributor.authorRussell, S
dc.contributor.authorShepherd, D
dc.date.accessioned2016-10-26T21:29:54Z
dc.date.available2016-10-26T21:29:54Z
dc.date.issued2012-08
dc.identifier.issn1534-5807
dc.identifier.issn1878-1551
dc.identifier.urihttp://hdl.handle.net/10026.1/6644
dc.description.abstract

Mechanisms of CNS repair have vital medical implications. We show that traumatic injury to the ventral midline of the embryonic Drosophila CNS activates cell divisions to replace lost cells. A pilot screen analyzing transcriptomes of single cells during repair pointed to downregulation of the microtubule-stabilizing GTPase mitochondrial Rho (Miro) and upregulation of the Jun transcription factor Jun-related antigen (Jra). Ectopic Miro expression can prevent midline divisions after damage, whereas Miro depletion destabilizes cortical β-tubulin and increases divisions. Disruption of cortical microtubules, either by chemical depolymerization or by overexpression of monomeric tubulin, triggers ectopic mitosis in the midline and induces Jra expression. Conversely, loss of Jra renders midline cells unable to replace damaged siblings. Our data indicate that upon injury, the integrity of the microtubule cytoskeleton controls cell division in the CNS midline, triggering extra mitosis to replace lost cells. The conservation of the identified molecules suggests that similar mechanisms may operate in vertebrates.

dc.format.extent433-440
dc.format.mediumPrint-Electronic
dc.languageen
dc.language.isoeng
dc.publisherElsevier BV
dc.subjectAnimals
dc.subjectCell Differentiation
dc.subjectDrosophila Proteins
dc.subjectDrosophila melanogaster
dc.subjectEnzyme Activation
dc.subjectMicrotubules
dc.subjectMitosis
dc.subjectProto-Oncogene Proteins c-jun
dc.subjectTubulin
dc.subjectrho GTP-Binding Proteins
dc.titleDisruption of Microtubule Integrity Initiates Mitosis during CNS Repair
dc.typejournal-article
dc.typeArticle
plymouth.author-urlhttps://www.ncbi.nlm.nih.gov/pubmed/22841498
plymouth.issue2
plymouth.volume23
plymouth.publication-statusPublished
plymouth.journalDevelopmental Cell
dc.identifier.doi10.1016/j.devcel.2012.06.002
plymouth.organisational-group/Plymouth
plymouth.organisational-group/Plymouth/Faculty of Health
plymouth.organisational-group/Plymouth/Faculty of Health/Peninsula Medical School
plymouth.organisational-group/Plymouth/REF 2021 Researchers by UoA
plymouth.organisational-group/Plymouth/REF 2021 Researchers by UoA/UoA01 Clinical Medicine
plymouth.organisational-group/Plymouth/REF 2021 Researchers by UoA/UoA03 Allied Health Professions, Dentistry, Nursing and Pharmacy
plymouth.organisational-group/Plymouth/Research Groups
plymouth.organisational-group/Plymouth/Research Groups/Institute of Translational and Stratified Medicine (ITSMED)
plymouth.organisational-group/Plymouth/Research Groups/Institute of Translational and Stratified Medicine (ITSMED)/CBR
plymouth.organisational-group/Plymouth/Users by role
plymouth.organisational-group/Plymouth/Users by role/Academics
plymouth.organisational-group/Plymouth/Users by role/Researchers in ResearchFish submission
dc.publisher.placeUnited States
dcterms.dateAccepted2012-06-04
dc.identifier.eissn1878-1551
dc.rights.embargoperiodNot known
rioxxterms.versionofrecord10.1016/j.devcel.2012.06.002
rioxxterms.licenseref.urihttp://www.rioxx.net/licenses/all-rights-reserved
rioxxterms.licenseref.startdate2012-08-14
rioxxterms.typeJournal Article/Review
plymouth.oa-locationhttp://www.cell.com/developmental-cell/pdf/S1534-5807(12)00275-4.pdf


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