A Database of Drosophila Genes & Genomes

FB2013_03, released May 7th, 2013
 

Allele Dmel\DlRevF10

General Information
SymbolDmel\DlRevF10SpeciesD. melanogaster
NameFlyBase IDFBal0029366
Feature typealleleAssociated geneDmel\Dl
Also Known AsDlrev10, DeltarevF10, Dlrev10e
Allele classloss of function allele, amorphic allele - genetic evidence
Mutagen
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Description
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FB2013_03
FB2013_02
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hide Nature of the Allele
Allele class
Mutagen
Mutations Mapped to the Genome
Type
Location
Additional Notes
References
Associated Sequence Data
DDBJ /
EMBL /
GenBank
DNA sequence
Protein sequence
Name
 
UniProtKB/Swiss-Prot
UniProtKB/TrEMBL
Progenitor genotype
Nature of the lesion
Statement
Reference
Excision of the promoter region, transcription start site and first exon.
Revertant of a P-element insertion located between -20 and -30 upstream of the Dl transcription start site. Deletion of approximately 760bp removing most of the first exon and the proximal part of the promoter (including the TATA box).
Cytology
hide Phenotypic Data
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hide Phenotype Manifest In
dorsal mesothoracic disc & sensory mother cell | dorsal/ventral compartment boundary
eye disc & neuron
scutum & macrochaeta | somatic clone
sensory mother cell & mesothoracic tergum & third instar larva | ectopic | somatic clone
hide Detailed Description
Statement
Reference
Clones of homozygous Dl[RevF10] mutant ovarian follicle cells tend to have larger nuclei than surrounding wild-type cells.
Homozygous clones in the outer proliferation center neuroepithelium (induced at late-first or early-second instar and analysed at late-third instar) adopt rounded or irregular cell morphology rather than the normal columnar epithelial cell morphology in 87.5% of cases.
Homozygous intestinal stem cell (ISC) clones in the adult midgut often grow into tumours, or into a tumour plus a single enterocyte (EC). Other homozygous ISC clones differentiate into a single EC.
DlRevF10 mutant germline stem cells differentiate and leave the niche, resulting in an empty germarium phenotype when both germline stem cells are mutant.
Clones of Dl[RevF10] mutant cells in a Minute/+ background in the position of the second mitotic wave of the eye disc do not enter S phase and do not undergo mitosis. However, occasional cells that incorporate BrdU (a marker of S phase) are observed in some Dl[RevF10] clones. Also, there is a rescue of the G1 block at the borders of the Dl[RevF10] clones.
DlRevF10 third instar nota clones exhibit at least eight sensory organ precursors (SOPs) in approximately 11% of SOP positions scored. Approximately 11% of SOP positions display between four and eight ectopic SOPs, while approximately 41% exhibit between one and four SOPs, with 37% exhibiting one SOP, as in wild-type.
Female flies heterozygous for DlRevF10 show thickened wing vein L3 and duplicated anterior and posterior scutellar macrochaetae.
Photoreceptor cells are absent from the centers but not the borders of DlRevF10 homozygous somatic clones in the eye disc. R8 photoreceptor cells cluster just inside the boundaries of these clones.
Heterozygotes show no effect on the notum macrochaetae.
Large clones in the eye disc that cross the morphogenetic furrow cause its anterior displacement.
No extra cell divisions are seen in homozygous follicle cell clones. In egg chambers containing homozygous germline clones, defects are seen in cell cycle regulation in follicle cells surrounding the germline clones. The follicle cells retain their normal apical-basal polarity in stage 8-9 egg chambers (some epithelial defects are seen in later egg chambers).
Sensory organ precursors (SOPs) at the prospective wing margin of third instar larval wing discs are lost in DlRevF10 somatic clones, except in cases where a cell within the clone abuts wild-type wing margin cells. There may be some non-autonomous effect of these clones on SOPs: 83% of the clones have wild-type (WT) SOPs next to DlRevF10 non-SOPs versus 14% with DlRevF10 SOPs next to WT non-SOPs, and almost no pairs of adjacent WT and DlRevF10 mutant SOPs (3%).
Somatic clones in the eye lead to defects. Ommatidia that are entirely DlRevF10 are grossly abnormal, as are the majority of mosaic ommatidia in which many of the cells are DlRevF10. However the remaining mosaic ommatidia develop a normal complement of photoreceptors. Notably almost none of these ommatidia contain mutant R8 cells and only a few contain mutant R2 or R5 cells. No ommatidia are seen that are mutant for both R1 and R6 cells. All other possible mosaic combinations of the R1/6/7 trio occur at frequencies similar to that in wild-type control clones.
Clones in the eye (located away from the dorsoventral midline) result in an excess of photoreceptors in the middle of the clone. At the margins of the clone, in ommatidia that are mosaic in the R3/R4 photoreceptors, the Dl+ cell always adopts the R3 fate. This can result in polarity reversals and inverted chirality. Ommatidia containing the normal number of photoreceptor cells in which the R3/R4 pair are mutant for DlRevF10 show an R3/R3 phenotype.
Homozygous DlRevF10 SerRX106 double mutant clones in the leg result in a failure to form joints. In most cases, the failure to form joints is an autonomous property of the mutant cells in the clone.
Homozygous clones induced early during eye development are associated with large abnormal patches of mutant tissue, with only rare mosaic ommatidia containing the normal number of 8 photoreceptors forming at the interface with wild-type tissue. Homozygous clones induced later during eye development can give rise to mosaic ommatidia with the normal number of photoreceptor cells. In those cases in which the R3/R4 pair is mosaic for DlRevF10, the mutant cell invariably develops as R4 and the wild-type cell develops as R3, irrespective of the location of the ommatidium within the eye, resulting in incorrect chiralities. In ommatidia in which both the R3 and R4 cells are mutant for Dl, the ommatidia can be symmetrical, or asymmetrical with the incorrect chiral form. The R8 cell body normally achieves an asymmetric position on the R3 rather than the R4 side of the ommatidium in wild-type flies. Frequent uncoupling of the R8 position from the R3/R4 asymmetry is seen in DlRevF10 mosaics. In these cases, R8 cells are usually found between R5/R6, occasionally found between R1/R6 and in rare cases are found between other cells.
The segmental border muscle progenitors do not segregate at all or do not divide properly.
Neural differentiation does not occur in DlRevF10 SerRX106 double mutant clones in the eye disc, except near the clone margins. Where neural differentiation occurs near the clone margins, excessive numbers of R8 cells are seen. This phenotype resembles that seen for clones homozygous for Dl- alone.
Homozygous clones on the adult scutum have a tuft of densely packed bristles in the interior of the clone. Homozygous clones induced in the sensory organ lineage produce largely normal external bristle structures, with only 5% of homozygous macrochaetae having double shafts. Homozygous clones in the wing lead to modest expansions of vein tissue into the intervein area.
Clonal cells in the eye disc are associated with neural hypertrophy involving clusters of R8 cells near the clone margin. Clones in the adult retina show ommatidia with excess photoreceptor cells only being found clone to the clone boundaries. Centre of the clone is undifferentiated or absent.
Homozygous embryos have an increased number of cardiac precursor cells.
In mutant embryos carrying Dlm39 segregation of neuroblasts 5-2 and 7-4 is normal at early stages. Embryos derived from germline clones exhibit disturbed segmentation in some segments and some 5-2 equivalence groups are fused. Segregation of the 5-2 and 7-4 neuroblast occurs in an irregular manner at later stages. Scer\GAL4arm.T:Hsim\VP16-mediated expression of DlScer\UAS.cHa fails to rescue the CNS and PNS differentiation defects: CNS shows an abnormal axonal scaffold and the PNS contains less cells that wild type. Each proneural cluster is neuralized from the very beginning of neurogenesis. Replacement of Dl zygotic expression using Scer\GAL4arm.T:Hsim\VP16-mediated expression of SerScer\UAS.cSa allows some rescue but the CNS is reduced at later stages. P precursors of the larvae PNS segregate as a group of cells, Scer\GAL4arm.T:Hsim\VP16-mediated expression of DlScer\UAS.cHa allows normal delamination of the individual cells.
Clonal analysis reveals that Dl is required for wing margin formation in the ventral but not the dorsal compartment. Sensory bristles on the anterior wing margin and the noninnervated hairs of the posterior wing margin are absent in clones (dorsal and ventral) that give rise to these structures. Clones also cause hypertrophy of wing veins.
Mutant clones fail to form bristles.
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Reference
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Statement
Reference
DlRevF10 has visible | somatic clone phenotype, non-enhanceable by heph03429
hideNOT suppressed by
Statement
Reference
DlRevF10 has visible | somatic clone phenotype, non-suppressible by heph03429
hideEnhancer of
Statement
Reference
DlRevF10/Dl[+] is an enhancer of visible | recessive phenotype of dx152
DlRevF10/Dl[+] is an enhancer of visible phenotype of edslH8/ed1X5
DlRevF10 is an enhancer of visible phenotype of Myt1GMR.PP
hideNOT Enhancer of
Statement
Reference
DlRevF10/Dl[+] is a non-enhancer of visible phenotype of Scer\GAL4en-e16E, kermitGS2053
DlRevF10 is a non-enhancer of cell polarity defective phenotype of pkpk.sev
DlRevF10 is a non-enhancer of visible phenotype of osGMR.PB
hideNOT Suppressor of
Statement
Reference
DlRevF10/Dl[+] is a non-suppressor of visible phenotype of Scer\GAL4en-e16E, kermitGS2053
DlRevF10 is a non-suppressor of cell polarity defective phenotype of pkpk.sev
DlRevF10 is a non-suppressor of visible phenotype of osGMR.PB
hideOther
Statement
Reference
hide Phenotype Manifest In
hideEnhanced by
Statement
Reference
DlRevF10 has sensory mother cell & mesothoracic tergum & third instar larva | ectopic | somatic clone phenotype, enhanceable by mib1EY09780
DlRevF10 has sensory mother cell & mesothoracic tergum & third instar larva | ectopic | somatic clone phenotype, enhanceable by neur1
DlRevF10 has sensory mother cell & mesothoracic tergum & third instar larva | ectopic | somatic clone phenotype, enhanceable by SerRX106
hideNOT Enhanced by
Statement
Reference
DlRevF10 has wing vein | somatic clone phenotype, non-enhanceable by heph03429
hideSuppressed by
Statement
Reference
DlRevF10, DlScer\UAS.cLa, SerRX106 has sensory mother cell & mesothoracic tergum & third instar larva | ectopic | somatic clone phenotype, suppressible by Scer\GAL4mat.αTub67C.T:Hsim\VP16
DlRevF10, SerRX106 has sensory mother cell & mesothoracic tergum & third instar larva | ectopic | somatic clone phenotype, suppressible by SerScer\UAS.cGa/Scer\GAL4mat.αTub67C.T:Hsim\VP16
DlRevF10 has sensory mother cell & mesothoracic tergum & third instar larva | ectopic | somatic clone phenotype, suppressible | partially by Scer\GAL4mat.αTub67C.T:Hsim\VP16/fngScer\UAS.cKa
DlRevF10 has sensory mother cell & mesothoracic tergum & third instar larva | ectopic | somatic clone phenotype, suppressible by SerRX106/SerScer\UAS.cGa/Scer\GAL4mat.αTub67C.T:Hsim\VP16
DlRevF10 has sensory mother cell & mesothoracic tergum & third instar larva | ectopic | somatic clone phenotype, suppressible by SerScer\UAS.cGa/Scer\GAL4mat.αTub67C.T:Hsim\VP16
hideNOT suppressed by
Statement
Reference
DlRevF10 has wing vein | somatic clone phenotype, non-suppressible by heph03429
hideEnhancer of
Statement
Reference
DlRevF10/Dl[+] is an enhancer of macrochaeta | ectopic phenotype of edslH8/ed1X5
DlRevF10/Dl[+] is an enhancer of ocellus phenotype of dx152
DlRevF10/Dl[+] is an enhancer of ommatidium phenotype of dshhs.sev.B
DlRevF10/Dl[+] is an enhancer of ommatidium phenotype of fzhs.sev
DlRevF10/Dl[+] is an enhancer of photoreceptor cell R4 phenotype of fzhs.sev
DlRevF10/Dl[+] is an enhancer of wing vein phenotype of dx152
DlRevF10 is an enhancer of eye phenotype of Myt1GMR.PP
hideNOT Enhancer of
Statement
Reference
DlRevF10/Dl[+] is a non-enhancer of wing hair phenotype of Scer\GAL4en-e16E, kermitGS2053
DlRevF10 is a non-enhancer of eye phenotype of osGMR.PB
DlRevF10 is a non-enhancer of ommatidium phenotype of pkpk.sev
hideSuppressor of
Statement
Reference
hideNOT Suppressor of
Statement
Reference
DlRevF10/Dl[+] is a non-suppressor of ommatidium phenotype of Scer\GAL4hs.2sev, nmoScer\UAS.cUa
DlRevF10/Dl[+] is a non-suppressor of wing hair phenotype of Scer\GAL4en-e16E, kermitGS2053
DlRevF10 is a non-suppressor of eye phenotype of osGMR.PB
DlRevF10 is a non-suppressor of ommatidium phenotype of pkpk.sev
hideOther
Statement
Reference
DlRevF10, Scer\GAL4mat.αTub67C.T:Hsim\VP16, SerRX106, SerScer\UAS.cGa has sensory mother cell & mesothoracic tergum & third instar larva | ectopic | somatic clone phenotype
DlRevF10, Ser[+]/SerRX82, eygM3-12/eyg[+] has eye phenotype
DlRevF10, SerRX82 has scutum & macrochaeta phenotype
DlRevF10/Dl[+], Ser[+]/SerRX82, eygM3-12 has eye phenotype
DlRevF10/Dl[+], SerRX82, eygM3-12/eyg[+] has eye phenotype
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Statement
Reference
Dl[RevF10], Ser[RX106] double mutant clones in the adult thorax exhibit external sensory cell loss and an excess of neurons. A Dl[RevF10] Ser[RX106] double mutant background suppresses the extra socket cell phenotype seen in AP-47[SHE-11] thorax clones, instead producing the external sensory cell loss and excess neurons seen in Dl[RevF10] Ser[RX106] double mutants.
Dl[RevF10]/+ enhances the wing vein thickening phenotype of dx[152] hemizygotes. The second and third tarsal segments of the forelegs are fused in 41% of the double mutants, a phenotype that is not seen in either dx[152] hemizygotes or Dl[RevF10]/+ animals. The double mutants show fusion of the ocelli in 37% of cases, compared to the 2% penetrance seen in dx[152] hemizygotes.
DlRevF10, SerRX82 mutant germline stem cells differentiate and leave the niche, resulting in an empty germarium phenotype when both germline stem cells are mutant.
Neural differentiation and the second mitotic wave are blocked in clones of cells in the eye disc simultaneously mutant for Dl[RevF10] and Ras85D[ΔC40B] in a Minute/+ background: mutant cells in the position of the second mitotic wave do not enter S phase and do not undergo mitosis, as in Dl[RevF10] clones. Co-overexpression of CycA[Scer\UAS.cWa], E2f[Scer\UAS.cNa] and Dp[Scer\UAS.cDa] (using Scer\GAL4[GMR.PF]) does not significantly rescue the S phase phenotype seen in Dl[RevF10] clones in a Minute/+ background.
DlRevF10 SerRX106 third instar nota clones exhibit at least eight sensory organ precursors (SOPs) in approximately 70.5% of SOP positions scored. Approximately 21.5% of SOP positions display between four and eight ectopic SOPs, while approximately 6% exhibit between one and four SOPs, with only 2% exhibiting one SOP, as in wild-type. Addition of the DlScer\UAS.cLa transgene, under the control of Scer\GAL4mat.αTub67C.T:Hsim\VP16 partially rescues the ectopic SOP phenotype, with approximately 8.5% of SOP positions exhibiting between four and eight SOPs. Addition of the SerScer\UAS.cGa transgene, under the control of Scer\GAL4mat.αTub67C.T:Hsim\VP16, partially rescues the ectopic SOP phenotype, with approximately 26% of SOP positions exhibiting between one and four SOPs. DlRevF10 fngScer\UAS.cKa third instar nota clones (under the regulation of Scer\GAL4mat.αTub67C.T:Hsim\VP16) exhibit at least eight sensory organ precursors (SOPs) in approximately 47% of SOP positions scored. Approximately 12.5% of SOP positions display between four and eight ectopic SOPs, while approximately 28% exhibit between one and four SOPs, with only 12.5% exhibiting one SOP, as in wild-type. DlRevF10 SerScer\UAS.cGa third instar nota clones (under the regulation of Scer\GAL4mat.αTub67C.T:Hsim\VP16) do not exhibit lateral inhibition defects in sensory organ precursor development. neur1 DlRevF10 third instar nota clones exhibit at least eight sensory organ precursors (SOPs) in approximately 50% of SOP positions scored. Approximately 35% of SOP positions display between four and eight ectopic SOPs, while approximately 15% exhibit between one and four SOPs. No SOP positions appeared wild-type. Therefore neur enhances the Dl lateral inhibition phenotype. mib1EY09780 DlRevF10 third instar nota clones exhibit at least eight sensory organ precursors (SOPs) in approximately 40% of SOP positions scored. Approximately 45% of SOP positions display between four and eight ectopic SOPs, while approximately 5% exhibit between one and four SOPs, with 10% exhibiting one SOP, as in wild-type. Addition of the DlScer\UAS.cLa transgene, to DlRevF10 SerRX106 double mutant third instar nota clones, under the control of Scer\GAL4mat.αTub67C.T:Hsim\VP16, partially rescues the ectopic SOP phenotype, with approximately 8.5% of SOP positions exhibiting between four and eight SOPs.
DlRevF10, SerRX82 transheterozygotes have normal sized eyes, but eygM3-12; DlRevF10, SerRX82 triple heterozygous flies have small eyes.
DlRevF10/+ increases the number of extra macrochaetae on the notum seen in ed1X5/edslH8 adults.
Clones mutant for both heph03429 and DlRevF10 have an autonomous thick veins phenotype and are associated with non-autonomous vein differentiation in neighbouring tissue, as occurs in DlRevF10 single mutant clones.
The proportion of symmetrical (R3/R3) ommatidia in the eyes of stanScer\UAS.cUa; Scer\GAL4sev.PM181 flies is significantly enhanced by heterozygosity for DlRevF10.
Expression of Dl::NΔECN.Scer\UAS under the control of Scer\GAL4byn-Gal4 in a DlRevF10 mutant background results in boundary cell differentiation throughout the entire large intestine.
DlRevF10,SerRX82 double mutant somatic clones in the follicle cells does not lead to any detectable phenotype.
NMcd5 DlRevF10 SerRX82 triple mutant clones do not develop microchaetae but produce epidermis. Macrochaetae in NMcd5 DlRevF10 double mutant clones develop as single bristles rather than as a neurogenic tuft.
Dominantly enhances the eye-polarity phenotype of fzhs.sev; most fzhs.sev ommatidia show R3/R3-type symmetry in a DlRevF10 heterozygous background. Dominantly enhances the eye-polarity phenotype of dshhs.sev.B.
DlRevF10,SerRX106 double mutant somatic clones in wing discs fail to respect the dorsal ventral boundary.
The number of ftz expressing MP2 neurons increases compared to wild-type (About 15 on each side of the midline, as compared to 2 in wild-type) in DlRevF10,SerRX82 homozygous embryos derived from DlRevF10,SerRX82 homozygous female germ-line clones (lacking both maternal and zygotic function). This is the same phenotype as seen in other Dl alleles alone.
DlRevF10 SerRX82 double mutant clones in the eye behave in the same way as DlRevF10 single mutant clones.
DlRevF10 SerRX82 double homozygous clones on the adult scutum produce epidermal cells but not external bristle structures. DlRevF10 SerRX82 double homozygous clones induced in the sensory organ lineage frequently have bristles with double shafts (approximately 44% of homozygous macrochaetae have double shafts). Loss of external sensory structures (balding) is also seen. DlRevF10 SerRX82 double homozygous clones in the wing produce larger and more frequent thickening of the veins compared to single mutant DlRevF10 homozygous clones.
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Reference
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Rescued by
Not rescued by
Comments
Neurogenic phenotype, rescued by Dlm39.
hide Stocks ( 1 )
Bloomington
hide Notes on Origin
Discoverer
Revertant.
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hide Synonyms & Secondary IDs ( 14 )
Reported As
Symbol Synonym
DeltaRevF10
Name Synonym
Secondary FlyBase IDs
  • FBal0044741
hide References ( 77 )
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hide Recent research papers ( 9 )
Couturier et al., 2012, Nat. Cell Biol. 14(2): 131--139
Endocytosis by Numb breaks Notch symmetry at cytokinesis. [FBrf0217937]
Xie et al., 2012, Dev. Biol. 363(2): 399--412
Drosophila Epsin's role in Notch ligand cells requires three Epsin protein functions: The lipid binding function of the ENTH domain, a single Ubiquitin interaction motif, and a subset of the C-terminal protein binding modules. [FBrf0217494]
Banks et al., 2011, PLoS ONE 6(3): e18259
The functions of auxilin and rab11 in Drosophila suggest that the fundamental role of ligand endocytosis in notch signaling cells is not recycling. [FBrf0213386]
Benhra et al., 2011, Curr. Biol. 21(1): 87--95
AP-1 Controls the Trafficking of Notch and Sanpodo toward E-Cadherin Junctions in Sensory Organ Precursors. [FBrf0212697]
Leonardi et al., 2011, Development 138(16): 3569--3578
Multiple O-glucosylation sites on Notch function as a buffer against temperature-dependent loss of signaling. [FBrf0214548]
Nicholson et al., 2011, Development 138(2): 251--260
Notch-dependent expression of the archipelago ubiquitin ligase subunit in the Drosophila eye. [FBrf0212669]
Okegbe and DiNardo, 2011, Development 138(7): 1259--1267
The endoderm specifies the mesodermal niche for the germline in Drosophila via Delta-Notch signaling. [FBrf0213233]
Poulton et al., 2011, Development 138(9): 1737--1745
The microRNA pathway regulates the temporal pattern of Notch signaling in Drosophila follicle cells. [FBrf0213494]
Wang et al., 2011, Dev. Biol. 350(2): 414--428
Notch signaling regulates neuroepithelial stem cell maintenance and neuroblast formation in Drosophila optic lobe development. [FBrf0212909]