P{lacW} insertion in the 5' untranslated region, 48bp upstream of the initiator ATG codon.
mitotic anaphase & nuclear chromosome
The mitotic index of mutant larval brains is 0.65, compared to 1.02 in wild-type brains. Mutant larval brain neuroblasts treated with colchicine often do not arrest in prometaphase (which occurs in wild-type neuroblasts in response to colchicine), but instead enter an anaphase-like state with separated sister chromatids.
Homozygous lethality occurs mainly during the pupal stages, with most homozygotes surviving through the third larval instar stage. No mitotic abnormalities are seen in post-cellularisation homozygous embryos. Sister chromatids remain attached in only 32% of mitotic figures in homozygous third larval instar brains incubated for 1 hour with colchicine, indicating that the spindle checkpoint has often been bypassed. In brains that have not been treated with colchicine, the percentage of homozygous mitotic cells with separated sister chromatids is much higher, and the percentage of mitotic cells in prophase or prometaphase is much lower than in wild type. There is a threefold reduction in mitotic index. A significant number of anaphase figures in homozygous brains are aberrant, with three major kinds of abnormalities being seen at high frequency; firstly, chromosome bridges extend between the two separating groups of chromosomes in many anaphases, secondly, lagging chromatids remain behind at the position of the metaphase plate while other chromosomes have migrated to positions near the poles and thirdly, extensive chromosome fragmentation is seen in many anaphases. Mitotic cells in homozygous brains undergo vastly elevated levels of apoptosis compared to wild type.
Lethality occurs during third instar larval or pupal stages. Mutants exhibit visible disc abnormalities: very small or no discs. Clones cannot be induced in wild type discs. In tergites, clones with normal size and but lower than expected frequency are recovered. Clones cannot be recovered in the wing disc.
BubR1k03113 is a suppressor | partially of abnormal cell cycle phenotype of cidT11-2/cidT22-4
BubR1k03113 is a suppressor | partially of abnormal mitotic cell cycle | embryonic stage phenotype of cidT11-2/cidT22-4
BubR1k03113 is a suppressor of abnormal mitotic cell cycle phenotype of sub131
BubR1k03113 is a suppressor of abnormal mitotic cell cycle phenotype of dupa3
BubR1k03113 is a suppressor of abnormal mitotic cell cycle phenotype of aspE3
BubR1k03113, sub131 has abnormal size | larval stage phenotype
BubR1k03113, sub131 has decreased cell number | larval stage phenotype
BubR1k03113, sub131 has decreased occurrence of cell division | larval stage phenotype
BubR1k03113 is a suppressor of brain | larval stage phenotype of sub131
BubR1k03113 is a suppressor of mitotic cell cycle phenotype of dupa3
BubR1k03113, sub131 has brain | larval stage phenotype
The presence of a BubR1k03113 mutant background suppresses the increased mitotic index phenotype associated with cidT11-2/cidT22-4 mutants. The number of cells delayed in prophase and prometaphase also decreases dramatically in double mutants, whereas the number of cells in anaphase shows a corresponding increase and is greater than controls. BubR1k03113 cidT11-2/cidT22-4 double mutants exhibit a mitotic index nearly double that of cidT11-2/cidT22-4 single mutants.
sub131, BubR1k03113 double mutant larval brains show a lower percentage of cells in mitosis (0.65) compared to sub131 mutant brains (2.66) or wild-type brains (1.32).
sub131, BubR1k03113 double mutant larval brains are slow growing, small, and contain fewer cells than BubR1k03113 mutants.
BubR1k03113 suppresses the aspE3 metaphase-arrest phenotype.
I. Kiss.
The P{lacW} insertions in BubR1k03113 and BubR1k06109 are at the same location within the BubR1 gene.
Precise excision of the P{lacW} insertion in BubR1k03113 results in complete reversion of the lethality and associated mitotic defects seen in BubR1k03113 homozygotes.
Complements: l(2)0531505315. Complements: vlc07022. Complements: l(2)0985109851. Complements: EcRk04314. Complements: l(2)09851k08138. Complements: l(2)k09848k09848. Complements: Src42Ak10108.