102A3 (determined by in situ hybridisation)
Polytene chromosomes normal (Bridges).
In(4)ciD is an inversion in which the promoter regions and first exons of pan and ci have been swapped. ciD consists of a hybrid gene in which the pan promoter drives expression of a ci protein that carries the N-terminal region of pan. The predicted protein product consists of the first 246 amino acids of pan fused in frame to ci, of which the first 13 N-terminal amino acids are missing.
Small inversion, breakpoints are located 5' to the transcription unit and 10kb 3' to the transcription unit.
Two insertions of 4.9kb, one in the BglII HaeIII fragment and the second in the KpnI XhoI fragment.
Small cytologically invisible inversion.
visible | adult stage (with cimCherry)
ciD/+ wings have a disrupted wing vein L4.
In heterozygotes, L4 is partially absent.
Wing vein L4 is truncated, and small amounts of ectopic wing vein are occasionally present. The posterior wing margin is fused to the alula, has larger bristles and is often nicked.
Heterozygotes show loss of wing margin bristles. This phenotype is dominantly enhanced by panS28.
Longitudinal wing vein 4 (L4) is shortened, some posterior row hairs are missing and the posterior wing margin is flattened in heterozygotes.
Double mutant phenotype with CrebA mutants is additive.
Keyhole structure of the larval foregut does not form.
Coordinate mutant.
Wing vein interruption.
Frequent gaps in the midsection of row 1 of tarsal bristles, though the terminal bristles are always present.
Mirror segmentation phenotype of embryos is not altered by wghs.PN.
Lack all longitudinal and transverse veins and affect morphogenesis of legs and eyes.
Segment polarity phenotype.
Dominant wing venation defect and recessive segmentation defect.
Neuronal cell fate remains unchanged.
Interruptions in the fourth wing vein and slightly spread wings.
Wings show interruptions of L4 in two places: proximal to and distal to anterior crossvein. L5 also shows distal interruption. L3 and L5 thick. Considerable plexus effect and knotting of veins. Wings broader, warped or concave upward, regularly extended and bent backward. Alula fused with and in same plane as blade of wing. Black dried haemolymph from axillary spiracle. Slight scalloping of inner wing margin, with hairs and tufts. Direction and extent of temperature effects depends on genetic background (Scharloo). In general, no overlapping of wild type. Inviable in combination with Ax/Ax or Ax/Y (House and Lutes, 1975). H/+ inhibits scalloping of ciD but greatly enhances L4 interruption (House, 1959). Fully dominant in triplo-4's (Sturtevant, 1936). Two doses of ciD reduce survival of triplo-4 flies (Parker, 1969). Homozygotes lethal in embryo (Hochman, 1971). Embryonic segment polarity disrupted; anterior portions of segments with their denticle belts duplicated in mirror-image fashion; posterior portions missing; each segment almost entirely covered with denticles (Nusslein-Volhard and Wieschaus, 1980). Fine hairs eliminated from dorsal abdominal segments; replaced with clear cuticle and socketed denticles (Orenic, Chidsey, and Holmgren, 1987). Embryonic CNS relatively normal (Patel et al., 1989). Genotype of oocyte with respect to ciD without effect on phenotype of progeny (Orenic et al.). ciD/l(4)102ABc dies as embryo, ciD/l(4)102ABb as embryo or larva; in ciD/ciCe-2 death usually delayed until pupal stage (Hochman, 1971). Survival of ci/ciD/Df(4)M101-63a argues for nonallelism or pseudoallelism of ci and ciD (Hochman, 1971). RK1.
ciD has visible | dominant phenotype, enhanceable by Scer\GAL4en-e16E/knUAS.cVa
ciD has wing vein L4 phenotype, enhanceable by Scer\GAL4en-e16E/knUAS.cVa
ciD has wing margin phenotype, suppressible by nej3
ciD has wing margin phenotype, suppressible by nejQ7
ciD has trichome of the posterior wing margin phenotype, suppressible by nej[+]/nej3
Scer\GAL4en-e16E, ciD, knUAS.cVa has wing vein L5 phenotype
Approximately 14% of AntpCtx/+;ciD/+ flies exhibit ectopic wings on the head. Flies showing an ectopic wing on the head almost always show a normal or slightly reduced eye, whereas flies with a head capsule-to-thorax transformation mostly have reduced or lost eyes.
Ninety percent of the eyes of AntpCtx/+;ciD/+ flies show a normal to weakly reduced eye phenotype.
When knScer\UAS.cVa is driven by Scer\GAL4en-e16E in a ciD background, the truncation of L4 is stronger than seen in ciD alone and L5 is partly missing.
Not allelic with ci, at least with respect to its lethality, since ciD/Df(4)M101-63a survives, whereas ci/Df(4)M101-63a is mutant (Hochman, 1965). Based on location, phenotype and complementation, ciD and Ce postulated to be part of a single complex (Orenic, Slusarski, Kroll and Holmgren, 1990).
Ruch, 18th Jan. 1932.
The expression of l(1)sc is unaltered in early homozygous mutant embryos.
Induced revertants of the ciD phenotype have molecular alterations in the ciD transcript demonstrating the transcripts involvement in the ci phenotype, wing vein interruption.
ciD is epistatic to hh11, smo1 and fu513.