l(1)3Bf << bk1 << crm << l(1)EA65 << bk2 << l(1)3Eb
Df(1)N-8/+ adult females show wing defects that include thickening of the longitudinal vein 5.
Df(1)N-8/+ females ectopically expressing Hsap\ATXN1LScer\UAS.T:Zzzz\FLAG under the control of Scer\GAL4hh.PU rarely survive to adult stage (less than 10%) and the survivors display severe wing defects including a further thickening of the vein L5 compared to Df(1)N-8/+ controls.
Heterozygotes show loss of wing margin and wing vein thickening.
Flies bearing Df(1)N-8 are generally smaller than wild-type flies and have a transient, slightly brown, eye phenotype shortly after eclosion.
Does not cause unconditional lethality in hybrid females when heterozygous with D.simulans chromosome.
Single cells from Df(1)N-8 embryos transplanted into the ventral neurogenic region of wild-type host embryos can give rise to both neural and epidermal cells.
Deficient embryos show an uninterpretable mutant midgut phenotype.
Homozygous embryos are very abnormal compared to wild-type. Midgut primordia do not fuse, and Malpighian tubules branch.
Heterozygosity for this deletion has no effect on the mutant ovarian phenotype of ovoD2.
Hyperplasia of replicating sensory precursors: due to an increased number of ectodermal cells being recruited as sensory precursor cells. Extra precursor cells are recruited beyond the normal time window for neurogenesis in the PNS.
Heterozygous females exhibit reduced viability and fertility.
Mohr, 7 Oct. 1918.