Imprecise excision of the P{EP} element, resulting in a 785bp deletion (nucleotides 32,514 to 33,299 of DS03910) that removes the putative transcription start site and 5' UTR of Dg. 15bp of the inverted repeat of the P-element are still present. An A to T mutation and a 2bp deletion is found at the distal breakpoint.
785bp deletion (nucleotides 32,514 to 33,299 of DS03910) resulting from the imprecise excision of P{EP}DgEP2241. 15bp of the inverted repeat of the P-element are still present. An A to T mutation and a 2bp deletion is found at the distal breakpoint.
Approximately 60% of DgO86/Dg248 flies have a "detached" crossvein phenotype, where the crossvein is gapped from both veins L4 and L5, while most of the remaining mutant flies have a "gapped" phenotype where there is a gap between the crossvein and either vein L4 or L5.
89% of eggs laid by Dg248/DgO86 females mated to wild-type males hatch.
Late second instar Dg248 larvae have one or more muscles frequently missing or misattached. Occasional additional muscle tissue is present.
Muscles from Dg248 mutants are hyper-contracted. The width of muscle 6/7 combined from Dg248 mutants is larger than controls, whereas the muscle length is reduced. Additionally sarcomere size is reduced, and generally more variable in size compared to controls.
Dg248 and Dg248/Dg323 mutant third instar larvae crawl normally.
Late second instar Dg248/Dg323 larvae have one or more muscles frequently missing or misattached. Occasional additional muscle tissue is present.
Sarcomere size is larger and more variable in Dg248/Dg323 larval muscles compared to controls.
Dg248 mutant embryos show normal cardiac cell alignment.
The apicobasal polarity of the follicle epithelium is disrupted in mutant follicle cell clones, with the mutant cells forming a multi-layer epithelium. There are also gaps in the epithelium. Egg chambers containing homozygous germline clones usually arrest at around stage 6 of oogenesis.
Dg248, mRpL34248 has follicle cell | somatic clone phenotype
Dg248, tw[+]/tw1 has muscle attachment site | third instar larval stage phenotype
Dg248, sli2 has cardioblast phenotype
Dg248/Dg[+], sli2 has cardioblast phenotype
One copy of P{mRpL34+t1.3} completely rescues the lethality and sterility of Df(2R)Dg323/Df(2R)Dg248 transheterozygotes. Thus the lethality of the Df(2R)Dg248 chromosome is not due to an effect on Dg, but is due to disruption of mRpL34.
One copy of P{mRpL34+t1.3} completely rescues the polarity defects of Df(2R)Dg248 homozygous follicle cell clones. Expression of DgScer\UAS.cDb under the control of Scer\GAL4da.G32 also rescues the polarity defects of Df(2R)Dg248 homozygous follicle cell clones. Thus the apical-basal polarity defect of the Df(2R)Dg248 chromosome is due to concomitant disruption of both mRpL34 and Dg.
