heterozygosity does not significantly affect the mitotic index in the adult midgut epithelium, as compared to controls.
clones (in adult mushroom body γ lobe) are deficient in axon (but not dendrite) pruning compared to wild type.
/+ third instar larvae do not show any decrease in the neuromuscular junction bouton number.
heterozygous mutants exhibit extreme sensitivity to 1-octen-3-ol. These flies survive for approximately 15 days when exposed to 0.5ppm 1-octen-3-ol, significantly lower than the 18 days-long survival span observed for exposed wild-type flies.
As in wild type, a bsk1
mutant neuroblast clone in the larval brain maintains a single neuroblast and consists of many neuronal progeny.
Single cell bsk1
clones in mushroom bodies have axons with wild type projections.
mutant embryos exhibit defective dorsal closure. F-actin cable formation in the peripheral amnioserosa is less prominent and the outer (ventral) edge of the peripheral amnioserosa is able to maintain a higher activity of filopodia.
Approximately 60% of bsk1
homozygous embryos shows a 'dorsal open' phenotype.
Mutant embryos have dorsal holes in the cuticle.
Homozygous embryos show a weak dorsal-open phenotype.
Homozygotes show a defect in dorsal closure.
Homozygous embryos show defects in dorsal closure.
Embryos exhibit a dorsal open phenotype.
Embryonic cuticle is partially closed in the dorsal posterior part. Removal of maternal and zygotic bsk
) results in a complete dorsal open phenotype.
Initial phases of dorsal closure are normal, but the first rows under the leading cell row of the dorsal edge show only a partial lengthening cell shape change or no cell shape change at all. The defect is more pronounced in anterior cells. Embryonic cuticle defect is temperature sensitive: At 18o
C egg lays show weaker phenotypes. Embryos derived from germline clones show an extreme dorsal open phenotype, with no cell shape change in leading row cells, and dorsal closure never initiates. This phenotype is rescuable by zygotic bsk+
. Homozygous clones in the eye reveal no abnormality.
Mutant embryos show a dorsal hole due to a defect in dorsal closure. Dorsoventral patterning is not defective.