P{PZ} insertion is located 28bp upstream of a putative transcription start site as determined by cDNA analysis.
100% of the eggs laid by Ras85D05703/Ras85De1B mothers have a single central dorsal appendage.
The Ras85D05703 mutant result in a significant reduction in the number of type I synaptic boutons compared with wild-type.
Homozygotes have no detectable eye defects.
A low percentage of egg chambers from homozygous females degenerate between stages 8 and 10. Some egg chambers contain too few nurse cells or fail to correctly position the developing oocyte within the egg chamber. Female transheterozygotes with Df(3R)by10 have rudimentary ovaries. All late stage egg chambers lack dorsal appendage structures and possess only a patch of chorion centered on the dorsal midline. Few eggs are laid, eggs appear ventralised but their overall shape is normal. Homozygous eyes exhibit slightly disrupted ommatidial array. Ras85DΔC17b/Ras85D05703 and Df(3R)ΔC40b/Ras85De1B transheterozygotes are lethal. Ras85De1B/Ras85D05703 and Ras85De2F/Ras85D05703 transheterozygotes are semi-lethal. Ras85DSutor-341/Ras85D05703 and Ras85DSutor-404/Ras85D05703 transheterozygotes have low viability. Female transheterozygotes with Ras85De2F, Ras85DSutor-341 or Ras85DSutor-404 lay eggs with a severely disrupted eggshell (patch of chorion instead of dorsal appendages), 57%, 40% and 25% of eggs (respectively) hatch and develop to normal larvae. Unhatched Ras85D05703/Ras85De2F embryos have normal cuticles, or are missing elements of the head skeleton or have defects in the anterior and posterior termini, holes in the cuticle and disordered posterior segments. Female transheterozygotes with Ras85De1B lay eggs with a single dorsal appendage, 84% of eggs hatch and develop to normal larvae. Transheterozygotes with Ras85De2F, Ras85DSutor-341 or Ras85DSutor-404 exhibit slightly disrupted ommatidial array (small number of fused and misplaced ommatidia). Transheterozygotes with Ras85De1B exhibit extremely rough eyes (many fused and misplaced ommatidia).
female-sterile.
Ras85D05703 is an enhancer of visible phenotype of RasGAP1EP45, Scer\GAL4hs.2sev
Ras85D05703 has phenotype, non-suppressible by Rlb1hs.PE
Ras85D05703/Ras85D[+] is an enhancer of heart primordium phenotype of sli2
Ras85D05703 is an enhancer of eye phenotype of RasGAP1EP45, Scer\GAL4hs.2sev
Ras85D05703/Ras85D[+] is a suppressor of phenotype of Src42ASu(Raf)1-1
Ras85D05703/+; sli2/+ embryos produce a mild heart development phenotype.
Dominantly suppresses the ability of Src42ASu(phl)1-1 to suppress the lethality of phl1/Y flies.
Expression of Gap1EP45 in homozygous Ras85D05703 flies using Scer\GAL4hs.2sev produces severely disorganised eyes.
Expression of Rlb1hs.PE fails to ameliorate the phenotype.
Ras85D05703 is rescued by Ras85D+t5.5
Ras85D05703 is not rescued by Ras85DΔ
Mutant phenotypes are completely rescued by Ras85D+t5.5, restoring viability and proper ovarian development. Ras85DΔ fails to rescue the mutant phenotypes.
A. Spradling.
Complements: ms(3)85D03565.
Precise excision of the P{PZ} insertion reverts the lethal and female sterile phenotypes demonstrating the insertion is responsible for the mutant phenotype.