|Feature type||allele||Associated gene||Dmel\Dl|
|Also Known As||Dl9p39|
|Allele class||amorphic allele - genetic evidence|
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|Nature of the Allele|
|Mutations Mapped to the Genome|
|Associated Sequence Data|
|Nature of the lesion|
|Phenotype Manifest In|
thorax & macrochaeta
Mutant embryos show a complete loss of pericardial cells and hematopoietic precursors, while cardioblast numbers are dramatically increased compared to wild type.
Dl[9P] mutant neuroectodermal cells transplanted into wild-type hosts do not affect cell fate changes in NB1-1, MP2 and NB7-1 lineages. RP2/RP2sib and vMP2/dMP2 cell fates are not correctly resolved in Dl[9P] mutants.
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.
Dl9P/DlRF animals shifted to the nonpermissive temperature during the early pupal stage develop double shaft bristles.
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.
Clusters of R8 cells develop in DlRF/Dl9P flies raised at the restrictive temperature. The clusters are not randomly arranged, but are based on the original R8 array.
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.
Double mutants Dl9P and dl2 had neuralization of additional ectodermal cells in the thoracic and abdominal segments. Double mutants Dl9P and Tl had neuralization of the entire ectoderm, a huge CNS and no epidermis as it had been substituted for by neural tissue.
Extreme embryonic neurogenic phenotype.
|NOT Enhanced by|
|Phenotype Manifest In|
|NOT Enhanced by|
Dl9P has presumptive embryonic/larval central nervous system phenotype, suppressible by H2
|NOT suppressed by|
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
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].
Flies that are homozygous for rumi44 and heterozygous for Dl9P show a synergistic increase in wing vein expansion.
The Dl9P thick vein phenotype is enhanced by Snr1E1, especially near the distal tips of veins L3, L4 and L5. The Dl9P thick vein phenotype is enhanced by Snr1E1/Snr1R3.
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.
frcNP0297 in double heterozygous combination with Dl9P results in duplications of the anterior scutellar bristles.
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.
Flies that are dxENU/Y; Su(dx)1/+; Dl9P/+ are viable but display clear dx phenotypes in the ocelli and wings.
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.
|Complementation & Rescue Data|
|Stocks ( 2 )|
|Notes on Origin|
The genotypes DlRF/DlRF, DlRF/Dl6B, and DlRF/Dl9P show a hypomorphic series, with DlRF/Dl9P showing the least function at any given restrictive temperature.
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|
|Synonyms & Secondary IDs ( 6 )|
(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, )
|Secondary FlyBase IDs|
|References ( 71 )|
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|Recent research papers ( 4 )|
|Recent reviews (0)|
|All reviews listed in FlyBase were published before 2011|