Spindle assembly checkpoint inactivation fails to suppress neuroblast tumour formation in aurA mutant Drosophila

被引：15
|
作者：
Caous, Renaud [1 ]
Pascal, Aude [1 ]
Rome, Pierre [1 ]
Richard-Parpaillon, Laurent [1 ]
Karess, Roger [2 ]
Giet, Regis [1 ]
机构：
[1] Univ Rennes 1, CNRS, UMR 6290, Inst Genet & Dev Rennes, F-35043 Rennes, France
[2] Univ Paris 07, Inst Jacques Monod, F-75205 Paris, France
来源：
NATURE COMMUNICATIONS | 2015年 / 6卷
关键词：
NEURAL STEM-CELLS; AURORA-A KINASE; CENTROSOME SEPARATION; ASYMMETRIC DIVISION; SELF-RENEWAL; CYCLIN B; IN-VIVO; COMPLEX; POLO; ORIENTATION;
D O I：
10.1038/ncomms9879
中图分类号：
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号：
07 ; 0710 ; 09 ;
摘要：
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.
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页数：9
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