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Título

Increased Aurora B activity causes continuous disruption of kinetochore-microtubule attachments and spindle instability

AutorMuñoz-Barrera, Marta; Monje-Casas, Fernando
Palabras claveIpl1
Sli15
INCENP
CPC
SAC
Fecha de publicación8-sep-2014
EditorNational Academy of Sciences (U.S.)
CitaciónProceedings of the National Academy of Sciences of the USA 111(38): E3996- E4005 (2014)
ResumenAurora B kinase regulates the proper biorientation of sister chromatids during mitosis. Lack of Aurora B kinase function results in the inability to correct erroneous kinetochore-microtubule attachments and gives rise to aneuploidy. Interestingly, increased Aurora B activity also leads to problems with chromosome segregation, and overexpression of this kinase has been observed in various types of cancer. However, little is known about the mechanisms by which an increase in Aurora B kinase activity can impair mitotic progression and cell viability. Here, using a yeast model, we demonstrate that increased Aurora B activity as a result of the overexpression of the Aurora B and inner centromere protein homologs triggers defects in chromosome segregation by promoting the continuous disruption of chromosome-microtubule attachments even when sister chromatids are correctly bioriented. This disruption leads to a constitutive activation of the spindle-assembly checkpoint, which therefore causes a lack of cytokinesis even though spindle elongation and chromosome segregation take place. Finally, we demonstrate that this increase in Aurora B activity causes premature collapse of the mitotic spindle by promoting instability of the spindle midzone.
Versión del editorhttp://dx.doi.org/10.1073/pnas.1408017111
URIhttp://hdl.handle.net/10261/123610
DOI10.1073/pnas.1408017111
Identificadoresdoi: 10.1073/pnas.1408017111
issn: 1091-6490
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