17kb deletion.

Deletion of ase and 17kb of flanking sequence.

Left breakpoint maps between coordinates -10.8 and -13.1 on the ASC map and right breakpoints between -25.8 and -30.7.

17-19 kb deletion between -11.5 and -30 Df(1)ase-1 mutation is a small deletion from coordinates -11.5 to -30 kb that includes the ase transcription unit, which is located at approximately coordinate -25 kb.

Df(1)ase-1 homozygotes present a significant decrease in the number of dividing neuroblasts during stage 14, but not stage 13, of embryogenesis, but show no significant difference in the number of dividing neuroblast daughters during stages 13 and 14 of embryogenesis, as compared to controls; these embryos, however, show no significant differences in the number of neuroblasts, as compared to controls.

The optic lobes of larvae that are hemizygous for Df(1)ase-1 contain ~45% fewer distal inner proliferation center (d-IPC) neuroblasts that contain dpn but not ato. The number of neuroblasts that express dpn and ato is only slightly reduced.

Mutant embryos show a low frequency (7% of segments) loss of one chordotonal organ from the lch5 lateral cluster of five chordotonal organs.

Mutants are viable and have normal bristle pigmentation.

Df(1)ase-1 flies have a reduced number of bristles on the anterior wing margin and abdomen, and some wing bristles show differentiation defects.

Number of glial cells in Df(1)ase-1 pupal wings is reduced by around 15%. At 13 hours AP several glial cells are evident, unlike for sc^10-1.

Reduction in number of wing bristles. Remaining bristles may develop abnormally giving rise to split shafts, multiple shafts or empty sockets. The orientation of remaining recurved bristles is often abnormal. Df(1)ase-1;hry¹ double mutants have four-fold fewer bristles in the L2 vein than hry¹ mutants alone.

Reduced viability. Reduced number of scutellar and abdominal bristles. Mechanosensory bristles of wing margin deformed, twinned and socketless bristles and bristleless sockets are all observed. Wing blade can be buckled in extremely affected cases. Embryos that lack ase are viable but are missing specific subset of sense organs.

Hemizygous males show a strong loss of chaetae on the tergite, with anterior and medial regions being devoid of chaetae. Homozygous females show an almost complete loss of tergite chaetae.

Not suppressed by su(Hw)² (E.B. Lewis in FBrf0020044) ase embryos lack a subset of peripheral neurons (FBrf0046281); third instar larvae show disrupted optic-lobe development; in adults almost all abdominal chaetae are removed as are the extra chaetae induced by Tft. Abdomen tends to be swollen; wings poorly expanded; viability of homozygous and hemizygous females low (FBrf0033191). Gene expression first detectable neural primordium, presumably in the neuroblasts. In later embryos, RNA is detected in most cells of the CNS primordium as well as in the labrum, optic lobe rudiment, procephalic neurogenic region and the posterior midgut rudiment. Expression lasts into germ-band retraction. Also expressed sparsely in third instar larvae; scarce in imaginal discs except for one large cell cluster in each leg disk; strong in the CNS, especially in a cap of cells over each optic lobe, which are destined to generate ganglion mother cells of the lamina and medulla; expression also seen in inner anlagen of optic lobes, which give rise to cells of the medulla and lobula complex. Otherwise expression in brain and ventral ganglion occurs in isolated clusters of cells and single cells. Expression thought to identify actively proliferating cells (FBrf0049898).

A. Garcia-Bellido.

Dubinin, 1928.

Df(1)ase-1 was formerly known as sc².

The adult phenotype, except for the mechanosensory bristle aspect, is due to a perturbation of the nearby sc gene: the defect is not complemented by sc^10-1. The mechanosensory bristle aspect of the phenotype is rescued by the P{ase-G:4.8} and P{ase-G:3.5} constructs. The ventral sensillum campaniformium phenotype is partly rescued.