Allele Dmel\Dl9P
| General Information | |||
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| Symbol | Dmel\Dl9P | Species | D. melanogaster |
| Name | FlyBase ID | FBal0002474 | |
| Feature type | allele | Associated gene | Dmel\Dl |
| Also Known As | Dl9p39 | ||
| Allele class | amorphic allele - genetic evidence | ||
| Mutagen | ethyl methanesulfonate | ||
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| Description |
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| FB2013_03 | |||
| FB2013_02 | |||
| All updates | Click here to see a list of all updates to this record from FB2010_08 and on. | ||
Nature of the Allele
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| Allele class | |||
| Mutagen | |||
| Mutations Mapped to the Genome | |||
Type Location Additional Notes References | |||
| Associated Sequence Data | |||
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EMBL / GenBank | DNA sequence Protein sequence Name | ||
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| Progenitor genotype | |||
| Nature of the lesion | Statement Reference Point mutation. | ||
| Cytology | |||
Phenotypic Data
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Phenotypic Class
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Phenotype Manifest In
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thorax & macrochaeta tormogen cell (with DlRF) | |||
Detailed Description
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Statement Reference Dl[9P]/+ flies display thickened wing veins (typically for veins L2 and L5). Mutant embryos show a complete loss of pericardial cells and hematopoietic precursors, while cardioblast numbers are dramatically increased compared to wild type. The accumulation of hemocytes is normal in the wings of heterozygous pupae, both at 22 and 26 hours after puparium formation.
Heterozygotes show wing vein thickening. 20% of heterozygotes have ectopic or duplicated macrochaetae. In Dl9P homozygous embryos, the early steps of proventricular development including the formation of the ball-like evagination at the ectoderm/endoderm boundary occur normally. However, at stage 14, the anterior boundary cells of the keyhole region fail to invaginate into the endodermal cell layer, but arrest anteriorly and do not move inwards until the final stages of embryonic development (16 and 17). In addition, the posterior boundary cells of the endodermal component of the proventriculus rim collapses in these animals. Heterozygotes display extra vein material particularly at the distal tip of veins. Homozygous mutant somatic clones in the notum give a phenotype of adjacent bristles with no intervening epidermal cells. A band of mutant epidermis, that averages about 4.2 cells wide around the clone, have a wild-type phenotype. Homozygous clones in the scutum produce a similar phenotype to homozygous DlRevF10 clones. Heterozygotes with SerBd-3 are viable and exhibit a severe wing phenotype. Instead of forming distinct invagination folds, the Dl mutant stomodeal nervous system anlage invaginates en masse. Thickened vein mutant. Hyperplasia of replicating sensory precursors: due to an increased number of ectodermal cells being recruited as sensory precursor cells. In double mutant clones with Nl1N-ts1, both wild type and mutant bristles are formed along the mosaic borders, and occasionally a mutant and a wild type bristle are found adjacent to each other (which never happens in either single mutant). Homozygous NAx-59b mutant clones develop as epidermis, and this requires Dl function. Clones in the thorax have an abnormal distribution of microchaetae and macrochaetae. Increase in SMCs per cluster in embryos lacking the maternal product. Mutant clones cause the differentiation of masses of adjacent microchaetae not separated by epidermal hairs. On the scutum cells adopt a neural fate. Mutant cells behave nonautonomously: cells produce epidermis only along the mosaic border where they are in contact with wild type cells. Severe "abruptex" phenotype. Capable of rescuing the lethality conferred by all negatively complementing Ax heteroallelic combinations, individuals display an Ax, not wild type, phenotype. Wing phenotype: wing vein 2 and the distal part of wing vein 5 are irregularly broadened. Other veins often form knots. All veins have pronounced deltas at the wing margin. Rough eye phenotype. Number of bristles in the thoracic segments is frequently increased. Homozygous clones in the eye and the cuticle are cell lethal. Extreme embryonic neurogenic phenotype. extreme allele | |||
External Data
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Interactions
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Phenotypic Class
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Enhanced by | |||
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NOT Enhanced by | |||
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Suppressed by | |||
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Enhancer of | |||
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Suppressor of | |||
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Phenotype Manifest In
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Enhanced by | |||
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NOT Enhanced by | |||
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Suppressed by | |||
Statement Reference | |||
NOT suppressed by | |||
Statement Reference | |||
Enhancer of | |||
Statement Reference Dl9P/Dl[+] is an enhancer of interommatidial bristle | ectopic phenotype of Scer\GAL4lz-gal4, sensScer\UAS.cNa Dl9P/Dl[+] is an enhancer of wing vein | ectopic phenotype of Scer\GAL4tub.PU, cswN308D.Scer\UAS.P\T | |||
Suppressor of | |||
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Other | |||
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Additional Comments
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Genetic Interactions
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Statement Reference The wing vein phenotype resulting from the expression of uif[asterisk.Scer\UAS] under the control of Scer\GAL4[A9] is enhanced by Dl[9P]. Ovarioles in aretQB/aretQB ; Dl9P/+ females form a single large egg chambers with many germline cells. The fusome appears as dots. Most egg chambers have more than 16 germline cells in aretQB/aretPD ; Dl9P/+ ovaries. Three classes of abnormal egg chambers are seen, which are present in roughly equal numbers. In the first class, a large number of germline cells of roughly equal size are enveloped by a single epithelium of follicle cells. The remaining two classes arise from partial fusion of separate cysts; no stalk cells can be detected and the follicle cell layers of different egg chambers remain in contact with each other. In the "anterior/posterior fusion" class, a well-defined linear organisation within individual ovarioles is maintained, and adjacent egg chambers are fused with each other at their anterior and posterior boundaries. In the "random fusion" class, egg chambers are positioned irregularly and can be closely apposed to multiple different egg chambers on lateral as well as on anterior and posterior surfaces. In both the partial fusion classes, each egg chamber contains an oocyte. In the anterior/posterior fusion class the oocyte is present at the posterior of the cyst and in the random fusion class the oocyte is either lateral or posterior relative to the overall polarity of the ovariole. The addition of Dl9P/+ to Gp150P8/Gp150k11120b animals increases the proportion of mutant ommatidia from 19.2% to 67.6%. The addition of Dl9P/+ to Gp150k11120b/+ animals increases the proportion of mutant ommatidia from 0.19% to 2.7%. the addition of one copy of ebiE4 enhances the dominant wing vein phenotype seen in Dl9P/+ animals. The combination of ebi1-334.GMR and Dl9P/+ leads to flies with a significantly rough eye phenotype. The combination of Dl9P and neurScer\UAS.cLa ( when driven by Scer\GAL4VMQ) produces a blistered wing phenotype. The combination of Dl9P and neurScer\UAS.cLa (when driven by Scer\GAL4VMQ) produces a blistered wing phenotype. Enhances the rough eye phenotype caused by expression of atoScer\UAS.cJa under the control of Scer\GAL4sca-109-68. The cuticle defect of homozygous embryos is not rescued by bibScer\UAS.cDa expressed under the control of Scer\GAL4h-1J3. Double mutants with Df(1)sc-B57 have normal midgut epithelium, but the large basophilic midgut cells are missing and the number of adult midgut precursor cells are reduced. Delta phenotype dominantly enhanced by Su(H)2. Dl9P flies carrying RpS32 in trans have an enhanced Dl wing phenotype and extremely rough eyes. Few flies of this genotype eclose. H2 reduces the central nervous system hypertrophy seen in Dl9P homozygous embryos. Double homozygous Dl9P H2 clones in the eye are viable, and are sometimes indistinguishable from wild-type. | |||
Xenogenetic Interactions
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Complementation & Rescue Data
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| Comments | |||
Stocks
( 2 ) | |||
| Bloomington | |||
| Kyoto | |||
Notes on Origin
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| Discoverer | Nusslein-Volhard. | ||
Comments
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dominantly suppressed by alleles of H and S and two Su(Dl) loci, and dominantly enhanced by alleles of Px, px, Ni, bs, net and 13 E(Dl) loci. Strong Dl allele. Autosomal repressor: suppress phenotypes of all viable "abruptex" alleles but not the lethality of the lethal "abruptex" alleles. | |||
External Crossreferences & Linkouts
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| Other Crossreferences | |||
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Synonyms & Secondary IDs
( 6 ) | |||
| Reported As | |||
| Symbol Synonym | 9P39 Delta9p Dl9p39 Dl9P39 (Renaud and Simpson, 2001, Ramain et al., 2001, Lai and Rubin, 2001, Barolo et al., 2000, Lecourtois and Schweisguth, 1998, Doherty et al., 1997, Sun and Artavanis-Tsakonas, 1997, Leviten and Posakony, 1996, Hartenstein et al., 1996, Hu et al., 1995, Baker and Zitron, 1995, Sturtevant and Bier, 1995, Tepass and Hartenstein, 1995, Fortini and Artavanis-Tsakonas, 1994, Simpson et al., 1993, Rhyu et al., 1994, Coyle-Thompson and Banerjee, 1993, Busseau et al., 1994, Simpson et al., 1992, Bodmer et al., 1993, de Celis et al., 1993, Bender et al., 1993, Heitzler and Simpson, 1993, Parks and Muskavitch, 1993, Baker and Rubin, 1992, Rao et al., 1991, Goriely et al., 1991, Heitzler and Simpson, 1991, Brand and Campos-Ortega, 1990, Xu and Artavanis-Tsakonas, 1990, Xu et al., 1990, de la Concha et al., 1988, Vassin and Campos-Ortega, 1987, Vassin et al., 1985, Dietrich and Campos-Ortega, 1984, Lehmann et al., 1983, Campos-Ortega, 1983, ) Dl9P Dl9p | ||
| Name Synonym | |||
| Secondary FlyBase IDs | |||
References
( 71 ) | |||
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Recent research papers ( 4 ) | |||
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Recent reviews (0)
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| All reviews listed in FlyBase were published before 2011 | |||
Recent Updates
External Crossreferences & Linkouts