Dysdet-1 homozygous larvae show decreased locomotion, namely decreased frequency of peristaltic waves.
Indirect flight muscle myofibril integrity is disrupted in 3-5 days old Dysdet-1 mutant flies, and this phenotype becomes significantly more penetrant in older animals (13-15 days). The myofibril defects are significantly suppressed when the flies are given food supplemented with either 2-acetyl-4(5)-tetrahydroxybutyl imidazole (THI) or THI oxime.
Overall activity of Dysdet-1 mutant flies is reduced compared to controls.
Myofibril integrity is disrupted in 3-5 days old Dysdet-1/Df(3R)Exel6184 mutant flies, and this phenotype becomes significantly more penetrant in older animals (13-15 days). The myofibril defects are significantly suppressed when the flies are given food supplemented with either 2-acetyl-4(5)-tetrahydroxybutyl imidazole (THI) or the S1P analog FTY720.
No obvious tergal depressor of trochanter (TDT) muscle fiber defect is observed in homozygous Dysdet-1 animals.
Homozygotes have a crossvein phenotype with incomplete penetrance and variable expressivity; 78% of mutant flies have at least one wing with a defective posterior crossvein. 39% of mutant wings have a complete posterior crossvein, 42% have a "gapped" phenotype (the crossvein is detached from either vein L4 or L5, but not both), 18% have a "detached" phenotype (the crossvein is detached from both L4 and L5) and 1% have a "point" phenotype (the crossvein is reduced to a point).
det1/Df(3R)Exel6184 transheterozygotes show a posterior crossvein phenotype with 100% penetrance. 18% of mutant wings have a complete posterior crossvein, 49% have a "gapped" phenotype and 33% have a "detached" phenotype.
det1/detEP3397 transheterozygotes show a posterior crossvein phenotype with 100% penetrance.
Homozygotes exhibit truncation of the posterior crossvein.
Posterior crossveins detached from longitudinals at one or both ends and may be absent. Wings occasionally folded back under or folded flat at middle. Eyes sometimes rough and bulging. Wings slightly spread. Bristles tend to break; scutellars occasionally doubled. RK3.
Dysdet-1 has posterior crossvein phenotype, enhanceable by dpps1
Dysdet-1, dpps1 has wing vein L4 phenotype