Amino acid replacement: K7A.
Two amino acids corresponding to the N-terminal KEN box of BubR1 are mutated in this transgene.
Amino acid replacement: E8A.
BubR1KEN.T:Disc\RFP-mRFP,BubR1k06109 mutant larval brains (third instar) do not show any growth defects and have normal number of neuroblast as well as the mitotic index, the rate of aneu- or polyploid brain cells is however increased compared to controls.
Aneuploidy is at wild-type levels in BubR1KEN.T:Disc\RFP-mRFP neuroblasts.
Colchicine fails to arrest BubR1KEN.T:Disc\RFP-mRFP cells in mitosis and premature sister chromatid separation is approximately 20-fold higher than in wild-type.
BubR1KEN.T:Disc\RFP-mRFP neuroblasts show no obvious defects in spindle structure or function. Stable spindles rapidly capture chromosomes and form robust K-fibers, often within 3 minutes of nuclear envelope breakdown, as in wild-type. Anaphase figures present normal symmetrical chromatids.
Mitotic timing is normal in BubR1KEN.T:Disc\RFP-mRFP cells.
BubR1KEN.mRFP1, BubR1k06109 has abnormal mitotic cell cycle | third instar larval stage phenotype, enhanceable by Sas-4s2214/Sas-4s2214
BubR1k06109/BubR1KEN.mRFP1 is an enhancer of abnormal mitotic cell cycle | third instar larval stage phenotype of Sas-4s2214
BubR1k06109/BubR1KEN.mRFP1 is a non-enhancer of neoplasia | third instar larval stage phenotype of aurA8839/aurA17961
BubR1KEN.mRFP1 is a suppressor of abnormal mitotic cell cycle phenotype of aspE3
BubR1KEN.mRFP1, cnnHK21 has lethal | pupal stage phenotype
BubR1KEN.mRFP1, cnnHK21 has abnormal mitotic cell cycle phenotype
BubR1KEN.mRFP1, mad2G6595 has abnormal mitotic cell cycle phenotype
BubR1k06109/BubR1KEN.mRFP1 is a non-enhancer of larval neuroblast | third instar larval stage | increased number phenotype of aurA8839/aurA17961
BubR1k06109/BubR1KEN.mRFP1 is a suppressor of larval neuroblast | increased number | third instar larval stage phenotype of Sas-4s2214
The increased neuroblast number and mitotic index seen in aurA8839/aurA17961 transheterozygote larvae is not enhanced by combination with BubR1KEN.T:Disc\RFP-mRFP,BubR1k06109 (the mitotic index in the double mutants is even slightly decreased), whereas the rate of ploidy defects is increased compared to either of the single gene mutants.
The increased brain neuroblast (NB) number observed in Sas-4s2214 mutant third instar larvae is fully suppressed by combination with BubR1KEN.T:Disc\RFP-mRFP,BubR1k06109 (the NB number in the double mutants is even lower than in wild-type controls and the brains are also smaller), while the rate of ploidy defects is strongly increased compared to either of the single gene mutants.
Co-expression of aldScer\UAS.cAa and BubR1KEN.T:Disc\RFP-mRFP under the control of Scer\GAL4mat.αTub67C.T:Hsim\VP16 results in almost complete abolition of chromosome movement during anaphase. Spindle appearance is sudden but extension is limited. The width of the metaphase plate and sister kinetochore separation appear normal.
The high mitotic density caused by aspE3 is reduced five-fold in BubR1KEN.T:Disc\RFP-mRFP aspE3 double mutants.
Double mutants of BubR1KEN.T:Disc\RFP-mRFP and cnnHK21 are pupal lethal with aneuploidy averaging 15%.
BubR1KEN.T:Disc\RFP-mRFP mad2G6595 double mutants are viable and fertile, with aneuploidy levels no higher than in the single mutants. Anaphase figures also appear normal in double mutants. The time from nuclear envelope breakdown to anaphase is markedly reduced (by 40%) compared to BubR1KEN.T:Disc\RFP-mRFP single mutant or wild-type cells and 30% reduced compared to mad2G6595 single mutants. This acceleration is accompanied by an earlier onset of CycB breakdown. In contrast, the gap from CycB breakdown to anaphase is relatively constant between the double mutant and controls.