Deletion derivative of P{PZ}rJ375 deleting D sequences.
adult cuticle & adult head | somatic clone
D87/Df(3L)Exel6120 transheterozygotes present a significant decrease in the number of dividing neuroblasts, but not of dividing neuroblast daughters, during stage 14 of embryogenesis, as compared to controls.
Targeting of dendrites to antennal lobe glomeruli occurs normally in antennal lobe projection neurons that are part of D87 homozygous somatic clones.
Approximately 40% of eggs derived from females containing homozygous germline clones fail to hatch. Of the non-hatching eggs, approximately 25% have significant chorion defects, including malformation or duplication of the dorsal appendages. Some of the mutant eggs have dorsal appendages that are thicker, shorter and more widely spaced than normal, while others have 3 or 4 dorsal appendages.
The formation of neuroblasts NB1-1 and NB5-3 is hardly affected in D87 single mutant embryos (2% and 1% loss respectively).
NB 6-1 is not formed in 7.9% of hemisegments, NB 4-1 is not formed in 30.9% of thoracic hemisegments and RP2 is not formed in 12.9% of hemisegments.
Mutant embryos show a misplacement and loss of midline glia.
Somatic clones induced during the first and second instar have not been recovered in adults. Somatic clones induced during the third instar appear morphologically normal. Large clones are never detected in the head capsule or legs. Small patches of black necrotic cells are seen in the first antennal segment, the ventral head cuticle surrounding the eye and the leg tibial/tarsal boundary region.
Embryos exhibit severe segmentation defects, including loss or fusion of abdominal denticle belts (does not correspond to a segmentally repeated pattern). Also exhibit defects in the organisation of head structures. Thoracic segments appear largely unaffected. Embryos exhibit severe and variable defects in CNS organisation; fusions between several adjacent neuromeres resulting in 3-4 fewer ganglia, moderate to severe narrowing of the longitudinal axon connectives in some segments and fusion of the anterior and posterior axon commissures.
D87 has abnormal neuroanatomy phenotype, enhanceable by ind[+]/ind16.2
D87 has abnormal neuroanatomy phenotype, enhanceable by ind[+]/indRR108
D87 is a suppressor of visible phenotype of upd1GMR.PB
D87, vndD38 has abnormal neuroanatomy phenotype
D87 has neuroblast NB5-3 phenotype, enhanceable by SoxNGA1192
D87 has neuroblast NB1-1 phenotype, enhanceable by SoxNGA1192
D87 has larval RP2 motor neuron phenotype, enhanceable by ind[+]/ind16.2
D87 has larval RP2 motor neuron phenotype, enhanceable by ind[+]/indRR108
D87 is an enhancer of neuroblast NB5-3 phenotype of SoxNGA1192
D87 is an enhancer of neuroblast NB1-1 phenotype of SoxNGA1192
D87 is a suppressor of eye phenotype of upd1GMR.PB
D87, vndD38 has neuroblast NB6-1 phenotype
D87, vndD38 has neuroblast NB4-1 phenotype
The NB1-1 neuroblast fails to form in 48% of hemisegments in D87 SoxNGA1192 double mutant embryos. The NB5-3 neuroblast fails to form in 25% of hemisegments in D87 SoxNGA1192 double mutant embryos.