7.6kb insertion of the 412 element within the region encoding the eleventh cadherin domain very close to the 3' end of the fifth exon. Analysis of cDNAs reveals that the wild type splice donor of the fifth intron is inactivated by the insertion. As a result three cryptic splice donor sites are uncovered, two upstream of and close to the 412 and a third site 30bp within the 412 element. The result is that two out of three of these variants encode a product which is deleted for just 23 amino acids of the eleventh cadherin domain.
axon & larval optic lobe
glial cell & larval optic lobe
tarsal segment (with ds38k)
tarsal segment (with ds05142)
The wings of ds1 homozygote adults are slightly smaller and rounder than in controls, and have vein and hair patterning defects.
Scaffold axons project aberrantly in the larval optic lobes if ds1 mutants. Glia line these aberrant pathways and accumulate in abnormal destinations such as the lobula cortex.
Viable allele. In addition to 100% penetrant defects in leg, wing and thorax, rough patches in the eye appear at low frequency. Anterior crossvein is displaced posteriorly.
Wings shorter, blunter and broader; crossveins uniformly very close together. Abdomen and legs chunky. Slight dominance of close crossveins. Stronger alleles may exhibit enhanced dominance, reduced viability, female sterility, delayed emergence, widely spaced scutellar bristles and erect costal bristles. Strong interaction with d, fj and cg; double homozygotes often have excessive growth of thoracic parts and sometimes conversion of one organ into another (e.g., hypertrophy of notum, duplication of wings and antennae and transformations of tarsus to arista, eye to antenna or palpus, or wing to notum (Waddington, 1943; Waddington, 1962). Tarsal shortening enhanced by homozygous ssa and ssaB (Villee, 1945). RK1.
ds1/dsUAO71 has abnormal planar polarity phenotype, enhanceable by fjd1/fjd1
ds1/dsUAO71 is an enhancer of abnormal planar polarity phenotype of fjd1
ds1/dsUAO71, fjd1 has abnormal planar polarity phenotype
ds1/ds38k has tarsal segment phenotype, suppressible | partially by nkd2/nkd[+]
nkd2/+ partially suppresses the leg phenotype of ds38k/ds1 flies: tarsal joint formation is completely rescued and the size of the tarsal segments is recovered almost to that of wild type. dsh3/+ enhances the severity of leg phenotypes in ds05142/ds1 animals: The length of the segments is reduced and most of the tarsal joints very reduced or completely absent.
Unlike either single mutant, 'fjd1 ds1/fjd1 dsUAO71' flies completely lack a posterior crossvein and have defects in wing hair polarity. 16% of ommatidia in these double mutants are inverted compared to less than 1% in either single mutant. The wing shortening phenotype of fjd1 homozygotes is also enhanced by ds1/+. Like ds38k/dsUAO71 flies, ds38k/dsUAO71; fj109-583.Scer\UAS.T:Hsap\GALNT3 ; Scer\GAL4bi-omb-Gal4 flies have inverted ommatidia scattered throughout their eyes.
Bridges, 12th Nov. 1917.
Bridges.
ds1 is the weakest known allele.