Insertion of a 412 element 6 nucleotides into the second coding exon.
The overall architecture of the retina and lamina of the eye is not altered in homozygotes.
e1 mutants are defective in carcinine synthesis.
Photoreceptor terminals in e1 mutants exhibit a reduced number of synaptic vesicles. The density of these synaptic vesicles is approximately 75% of wild-type.
e1 flies do not exhibit ON and OFF transients in ERG recordings of the laminar LMC neurons at the onset and end of light stimulation.
Approximately 40% of HdcJK910 mutants show no visual alert response (to a moving block, than in wild-type freezes fly movement). Approximately 20% exhibit a delayed response, and a brief-pause response is observed in 24% of flies.
There are fewer synaptic vesicles per R1-R6 photoreceptor terminal in e1 mutants than in wild type.
A stripe of dark pigment seen in wild-type adult females near the posterior edge of abdominal segments A2-A6. e1 mutants retain a distinct pugment stripe and the cuticle anterior to the stripe is much darker than wild-type. In the thorax and wings, wild-type flies have a uniform colour. In e1 mutants the thorax and wings become more darkly pigmented, and new pigmentation patterns are seen.
N-Β-alanyldopamine levels are drastically reduced in homozygous flies compared to wild-type, while dopamine levels are elevated approximately twofold. When e1 pharate adult tissue is incubated with dopamine in vitro, the extent of inducible pigmentation of body cuticle, hairs and bristle sockets resembles that of wild-type, while pigmentation of the bristle shafts is significantly reduced.
A large fraction of homozygotes are arrhythmic with respect to locomotor activity when kept in constant darkness at 24oC, and the average signal-to-noise ratio (SNR) is lower than wild-type. Heterozygotes have intermediate SNR values between homozygotes and wild-type, indicating that their rhythmicity is not completely normal. Homozygotes usually show disorganised bouts of activity when transferred from a light-dark cycle to constant darkness. At 20oC, most homozygotes have weak rhythmicity or are arrhythmic, at 28oC, most homozygotes have significant periodicity. The circadian period tends to be shorter at 20oC and longer at 28oC. Some homozygotes have extremely weak rhythms under a light-dark cycle. Hemizygous e1/Df(3R)e-BS2 or e1/Df(3R)e-N19 flies show variable rhythmicity in constant darkness at 20oC and do not synchronise normally to light-dark cycles, similar to homozygotes. In contrast to homozygotes however, they do not show short-period rhythms at 20oC. norpA7 and norpA36 partially suppress the arrhythmicity of some homozygous e1 flies. The eclosion rhythm is normal.
Body colour: dark.
e1 is an enhancer of abnormal body color phenotype of Scer\GAL4pnr-MD237, yUAS.cCa
dysb[+]/Dysbe01028, e1 has abnormal locomotor behavior | dominant | adult stage phenotype
dysb[+]/Dysbe01028, e1 has abnormal courtship behavior | dominant | adult stage phenotype
e1, y1 has abnormal body color phenotype
e1, y1 has adult cuticle phenotype
e1/dysbe01028 heteroallelic mutants display locomotor hyperactivity and mating disorientation (loss of the strong male bias towards the courtship of females).
A stripe of dark pigment seen in wild-type adult females near the posterior edge of abdominal segments A2-A6. y1, e1 double mutants have brown pigment throughout the abdomen and the stripe is no longer distinct. In the thorax and wings, wild-type flies have a uniform colour. In y1 mutants these structures become tan. In e1 mutants the thorax and wings become more darkly pigmented, and new pigmentation patterns are seen. y1, e1 double mutants also show these patterns, but the black pigment is absent, and they consist of two shades of brown pigment.
Arose on: In(3R)C (inseparable).
According to Craymer in FBrf0063385, e1 was isolated on In(3R)C and was never successfully separated from it. Most ebony alleles denoted simply as "e" without a specific allele designation can be traced back to Muller's e4. Most ebony mutations in Stock Center stocks designated as e1 are probably e4.
Mutants have reduced amounts of histamine in the head.
Mutants are unable to synthesize β-alanyl-dopamine; they are deficient for the activity of β-alanyl-dopamine-synthase.