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dc.contributor.authorHégarat, N
dc.contributor.authorCrncec, A
dc.contributor.authorSuarez Peredo Rodriguez, MF
dc.contributor.authorEchegaray Iturra, F
dc.contributor.authorGu, Y
dc.contributor.authorBusby, O
dc.contributor.authorLang, PF
dc.contributor.authorBarr, AR
dc.contributor.authorBakal, C
dc.contributor.authorKanemaki, MT
dc.contributor.authorLamond, AI
dc.contributor.authorNovak, B
dc.contributor.authorLy, T
dc.contributor.authorHochegger, H
dc.date.accessioned2020-07-06T15:21:37Z
dc.date.issued2020-06-02
dc.identifier.citationThe EMBO journal, 2020, 39 (11), pp. e104419 - ?
dc.identifier.issn0261-4189
dc.identifier.urihttps://repository.icr.ac.uk/handle/internal/3817
dc.identifier.eissn1460-2075
dc.identifier.doi10.15252/embj.2020104419
dc.description.abstractTwo mitotic cyclin types, cyclin A and B, exist in higher eukaryotes, but their specialised functions in mitosis are incompletely understood. Using degron tags for rapid inducible protein removal, we analyse how acute depletion of these proteins affects mitosis. Loss of cyclin A in G2-phase prevents mitotic entry. Cells lacking cyclin B can enter mitosis and phosphorylate most mitotic proteins, because of parallel PP2A:B55 phosphatase inactivation by Greatwall kinase. The final barrier to mitotic establishment corresponds to nuclear envelope breakdown, which requires a decisive shift in the balance of cyclin-dependent kinase Cdk1 and PP2A:B55 activity. Beyond this point, cyclin B/Cdk1 is essential for phosphorylation of a distinct subset of mitotic Cdk1 substrates that are essential to complete cell division. Our results identify how cyclin A, cyclin B and Greatwall kinase coordinate mitotic progression by increasing levels of Cdk1-dependent substrate phosphorylation.
dc.formatPrint-Electronic
dc.format.extente104419 - ?
dc.languageeng
dc.language.isoeng
dc.publisherWILEY
dc.rights.urihttps://creativecommons.org/licenses/by/4.0
dc.titleCyclin A triggers Mitosis either via the Greatwall kinase pathway or Cyclin B.
dc.typeJournal Article
dcterms.dateAccepted2020-03-25
rioxxterms.versionofrecord10.15252/embj.2020104419
rioxxterms.licenseref.urihttps://creativecommons.org/licenses/by/4.0
rioxxterms.licenseref.startdate2020-06
rioxxterms.typeJournal Article/Review
dc.relation.isPartOfThe EMBO journal
pubs.issue11
pubs.notesNot known
pubs.organisational-group/ICR
pubs.organisational-group/ICR/Primary Group
pubs.organisational-group/ICR/Primary Group/ICR Divisions
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Cancer Biology
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Cancer Biology/Dynamical Cell Systems
pubs.publication-statusPublished
pubs.volume39
pubs.embargo.termsNot known
icr.researchteamDynamical Cell Systems
dc.contributor.icrauthorBakal, Christopher


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