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Mitotic regulation by Polo-like kinase 1 and the Chromosomal Passenger Complex

Ahonen, Leena (2008-11-21)

dc.contributorDepartment of Medical Biochemistry and Genetics, and Turku Graduate School of Biomedical Sciencesen
dc.contributor.authorAhonen, Leena
dc.date.accessioned2008-11-06T10:51:19Z
dc.date.available2008-11-06T10:51:19Z
dc.date.issued2008-11-21
dc.identifier.isbnISBN 978-951-29-3735-6
dc.identifier.urihttp://www.utupub.fi/handle/10024/42604
dc.description.abstractDuring mitosis, the duplicated genome must be accurately divided between two daughter cells. Polo-like kinase 1 (Plk1) and Aurora B kinase, together with its binding partners Incenp, Survivin and Borealin (chromosomal passenger complex, CPC), have key roles in coordinating mitotic events. The accuracy of cell division is safeguarded by a signaling cascade termed the mitotic spindle checkpoint (SC), which ensures that chromosomes are not physically separated before correct bipolar attachments have been formed between kinetochores and spindle microtubules (MT). An inhibitory “wait anaphase” signal, which delays chromosome separation (anaphase onset), is created at individual kinetochores and broadcasted throughout the cell in response to lack of kinetochore-microtubule (kMT) attachment or proper interkinetochore tension. It is believed that the fast turnover of SC molecules at kinetochores contributes to the cell’s ability to produce this signal and enables rapid responses to changing cellular conditions. Kinetochores that lack MT attachment and tension express a certain phosphoepitope called the 3F3/2 phosphoepitope, which has been linked to SC signaling. In the experimental part, we investigated the regulation of the 3F3/2 phosphoepitope, analyzed whether CPC molecules turn over at centromeres, and dissected the mitotic roles of the CPC using a microinjection technique that allowed precise temporal control over its function. We found that the kinetochore 3F3/2 phosphoepitope is created by Plk1, and that CPC proteins exhibit constant exchange at centromeres. Moreover, we found that CPC function is necessary in the regulation of chromatid movements and spindle morphology in anaphase. In summary, we identified new functions of key mitotic regulators Plk1 and CPC, and provided insighs into the coordination of mitotic events.en
dc.language.isoeng-
dc.publisherfi=Turun yliopisto|en=University of Turku|en
dc.relation.ispartofseriesTurun yliopiston julkaisuja. Sarja D, Medica – Odontologica
dc.subject.meshPhosphorylationen
dc.subject.meshProtein Kinases --metabolismen
dc.subject.meshKinetochoresen
dc.subject.meshChromosomal Proteins, Non-Histoneen
dc.subject.meshMitosisen
dc.titleMitotic regulation by Polo-like kinase 1 and the Chromosomal Passenger Complexen
dc.type.ontasotfi=Artikkeliväitöskirja|en=Doctoral dissertation (article-based)|
dc.identifier.urnURN:ISBN:978-951-29-3735-6
dc.relation.issn2343-3213
dc.description.notificationSiirretty Doriasta
dc.contributor.facultyfi=Lääketieteellinen tiedekunta|en=Faculty of Medicine|
dc.format.contentfulltext
dc.relation.numberinseries828-


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