Spindle assembly checkpoint inactivation fails to suppress neuroblast tumour formation in aurA mutant Drosophila
Renaud Caous,
Aude Pascal,
Pierre Romé,
Laurent Richard-Parpaillon,
Roger Karess and
Régis Giet ()
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Renaud Caous: Institut de Génétique et Développement de Rennes-Université de Rennes I-CNRS- UMR 6290
Aude Pascal: Institut de Génétique et Développement de Rennes-Université de Rennes I-CNRS- UMR 6290
Pierre Romé: Institut de Génétique et Développement de Rennes-Université de Rennes I-CNRS- UMR 6290
Laurent Richard-Parpaillon: Institut de Génétique et Développement de Rennes-Université de Rennes I-CNRS- UMR 6290
Roger Karess: Institut Jacques Monod-Université Paris Diderot-Paris 7
Régis Giet: Institut de Génétique et Développement de Rennes-Université de Rennes I-CNRS- UMR 6290
Nature Communications, 2015, vol. 6, issue 1, 1-9
Abstract:
Abstract Tissue homeostasis requires accurate control of cell proliferation, differentiation and chromosome segregation. Drosophila sas-4 and aurA mutants present brain tumours with extra neuroblasts (NBs), defective mitotic spindle assembly and delayed mitosis due to activation of the spindle assembly checkpoint (SAC). Here we inactivate the SAC in aurA and sas-4 mutants to determine whether the generation of aneuploidy compromises NB proliferation. Inactivation of the SAC in the sas-4 mutant impairs NB proliferation and disrupts euploidy. By contrast, disrupting the SAC in the aurA mutant does not prevent NB amplification, tumour formation or chromosome segregation. The monitoring of Mad2 and cyclin B dynamics in live aurA NBs reveals that SAC satisfaction is not coupled to cyclin B degradation. Thus, the NBs of aurA mutants present delayed mitosis, with accurate chromosome segregation occurring in a SAC-independent manner. We report here the existence of an Aurora A-dependent mechanism promoting efficient, timed cyclin B degradation.
Date: 2015
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Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:6:y:2015:i:1:d:10.1038_ncomms9879
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DOI: 10.1038/ncomms9879
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