Vps18, EG:171E4.1 , Dof, l(1)7
Gene model reviewed during 5.42
Gene model reviewed during 5.39
Gene model reviewed during 5.45
Gene model reviewed during 5.52
There is only one protein coding transcript and one polypeptide associated with this gene
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\dor using the Feature Mapper tool.
dor protein colocalizes with internalized dextran beads for a limited time in endocytic compartments in third larval instar garland cells. dor protein partially colocalizes with hk protein and with internalized dextran beads to endosomes in Schneider2:Sev cells. hk protein is confined to the perimeter of the large endosomes while dor protein is found in the interior as well.
GBrowse - Visual display of RNA-Seq signalsView Dmel\dor in GBrowse 2
Please Note This section lists cDNAs and ESTs that fall within the genomic extent of the gene model, which may include cDNAs and ESTs of genes within introns, or of overlapping genes. Please see GBrowse for alignment of the cDNAs and ESTs to the gene model.
For each fully sequenced cDNA the DGRC maintains various forms of the cDNA (e.g tagged or untagged) in several different host vectors for subsequent cloning and expression in Drosophila and Drosophila cell lines.
Mutants can be arranged in a linear sequence of increasing strengths; heterozygotes between different pairs of alleles show intermediate phenotypes; no evidence of interallelic complementation (Bischoff and Lucchesi, 1971). Recombinational mapping by Bischoff (1973) established the order illustrated in Lindsley and Zimm (1992) p.164.
dsRNA has been made from templates generated with primers directed against this gene.
dsRNA made from templates generated with primers directed against dor that is transfected into S2 treated with Listeria monocytogenes reveals a vacuolar escape phenotype in which the bacterial protein listeriolysin O is not required.
dsRNA made from templates generated with primers directed against this gene tested in RNAi screen for effects on Kc167 and S2R+ cell morphology.
dor has been located within a puff on the telomeric chromosome of D.funebris, D.virilis, D.hydei, D.repleta, D.mercatorum and D.paranaensis, within a puff on the distal part of the X chromosome of D.kanekoi and within a puff on the proximal portion of the X chromosome of D.pseudoobscura.pseudoobscura.
Lesions in dor reduce or eliminate pigmentation in the eyes and ocelli and block pigmentation of the fat body and tubules: dor is required for normal pigmentation of all four tissues.
Lethal dor allele belongs to the class of ecdysone deficient mutations.
dor mutants affect a number of developmental processes; severity of effect increases with increasing developmental temperature. Eye color orange, shade depending on allele and temperature. dor reduces eye pigmentation in combination with either cn or v or with bw, indicating reduction in both drosopterins and xanthommatin. Biochemical analyses show xanthommatin and five drosopterins to be reduced to different degrees in dor; levels, but not relative proportions, change according to temperature of development (Counce, 1957) (Puckett and Petty, 1980). Reciprocal transplantation experiments show that eye color is autonomous (Hadorn and Counce). dor females produce no progeny in crosses to dor males at 25oC, although some allelic combinations able to produce progeny at 18oC; and a few dor/+ daughters are produced in crosses to + males. Germ-line clones homozygous for the lethal allele dor28 produce collapsed eggs (Perriman, Egstrom and Mahowald, 1989). The lethal embryos produced by dor mothers reach gastrulation or beyond (Hildreth and Lucchesi, 1967; Counce, 1969). Maternal effect shown to be germ line autonomous by both ovarian (Garen and Gehring, 1972) and pole-cell transplantation (Marsh, van Deusen, Wieschaus and Gehring, 1977). Maternal lethal effect rescuable by injections into preblastoderm embryos of cytoplasm from unfertilized eggs of normal females (Garen and Gehring, 1972); dor+ substance present during early stages of vitellogenesis but not detected in yolk of cellular blastoderm embryos (Marsh et al., 1977). Abnormalities of dor cells in culture eliminated by extracts of normal post- but not pregastrulation embryos (Kuroda, 1977). dor males show variable extents of gonadal dysgenesis depending on culture conditions and genotypic background; abnormalities range from failure of testes to attach to genital ducts to failure of one attached testis to elongate (Lucchesi, Counce and Hildreth, 1968). Viability and longevity of dor homozygotes and hemizygotes variably reduced depending on allele and temperature; dor8 larvae develop melanotic pseudotumors (Stark, 1918; Oftedal, 1953) and midgut occlusion (Russell, 1940), dying in late third instar (Bischoff and Lucchesi, 1971). dor/dor8 lethal at 29oC (Belyaeva, Aizenzon, Semeshin, Kiss, Koczka, Baritcheva, Gorelova, and Zhimulev, 1980). dor in combination with ry, ry2 (Lucchesi, 1968) and car (Nash, 1971) causes lethality in pupal stage. Recovery of gynandromorphs with dor car male sectors less than in controls; bilateral gynandromorphs not observed, but distribution of male tissue resembles that of control (Grell, 1976). dor behaves as a semi-lethal in combination with pd and with cn bw (Lucchesi, 1968).