Open Close
General Information
Symbol
Dmel\DlRevF10
Species
D. melanogaster
Name
FlyBase ID
FBal0029366
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
Dlrev10, DeltarevF10, Dlrev10e
Key Links
Mutagen
    Nature of the Allele
    Mutagen
    Mutations Mapped to the Genome
     
    Type
    Location
    Additional Notes
    References
    Associated Sequence Data
    DNA sequence
    Protein sequence
     
     
    Progenitor genotype
    Cytology
    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).

    Expression Data
    Reporter Expression
    Additional Information
    Statement
    Reference
     
    Marker for
    Reflects expression of
    Reporter construct used in assay
    Human Disease Associations
    Disease Ontology (DO) Annotations
    Models Based on Experimental Evidence ( 0 )
    Disease
    Evidence
    References
    Modifiers Based on Experimental Evidence ( 1 )
    Disease
    Interaction
    References
    Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
     
    Disease-implicated variant(s)
     
    Phenotypic Data
    Phenotypic Class
    Phenotype Manifest In

    eye disc & neuron

    scutum & macrochaeta | somatic clone

    Detailed Description
    Statement
    Reference

    In DlRevF10 heterozygotes, the pupal notum shows a disordered pattern in the interval between proneural stripes one and five.

    DlRevF10 heterozygous adults show mild but significant increase in the number of the scutellar bristles compared to wild-type flies and also display ectopic wing vein material.

    Under control conditions, DlRevF10 adult posterior midgut clones show a significant increase in cell number in both males and females, as compared to control clones.

    Clones of homozygous DlRevF10 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.

    Flies heterozygous for DlRevF10 have smaller eyes than wild-type flies, but their head capsule appears of normal size.

    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 DlRevF10 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 DlRevF10 clones. Also, there is a rescue of the G1 block at the borders of the DlRevF10 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.

    External Data
    Interactions
    Show genetic interaction network for Enhancers & Suppressors
    Phenotypic Class
    Enhanced by
    NOT Enhanced by
    Statement
    Reference

    DlRevF10 has visible | somatic clone phenotype, non-enhanceable by heph03429

    Suppressed by
    Statement
    Reference

    DlRevF10 has abnormal size | dominant phenotype, suppressible by crb11A22/crb[+]

    NOT suppressed by
    Enhancer of
    Statement
    Reference

    DlRevF10/Dl[+] is an enhancer of visible | adult stage phenotype of Sirt12A-7-11

    DlRevF10/Dl[+] is an enhancer of visible phenotype of Caf1-105NIG.12892R, Scer\GAL4ey.PH

    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

    NOT Enhancer of
    Statement
    Reference
    Suppressor of
    Statement
    Reference

    DlRevF10/Dl[+] is a suppressor | partially of visible | heat sensitive phenotype of Dcr-2UAS.cDa, EogtGD5084, Scer\GAL4en.PU

    NOT Suppressor of
    Statement
    Reference

    DlRevF10/Dl[+] is a non-suppressor of visible phenotype of Scer\GAL4en-e16E, kermitGS2053

    DlRevF10 is a non-suppressor of visible phenotype of upd1GMR.PB

    DlRevF10 is a non-suppressor of abnormal cell polarity phenotype of pkpk.sev

    Other
    Phenotype Manifest In
    Enhanced by
    NOT Enhanced by
    Statement
    Reference

    DlRevF10 has wing vein | somatic clone phenotype, non-enhanceable by heph03429

    Suppressed by
    NOT suppressed by
    Enhancer of
    Statement
    Reference

    DlRevF10/Dl[+] is an enhancer of eye phenotype of Caf1-105NIG.12892R, Scer\GAL4ey.PH

    DlRevF10/Dl[+] is an enhancer of wing vein phenotype of dx152

    DlRevF10/Dl[+] is an enhancer of ocellus phenotype of dx152

    DlRevF10/Dl[+] is an enhancer of macrochaeta | ectopic phenotype of edslH8/ed1X5

    DlRevF10 is an enhancer of eye phenotype of Myt1GMR.PP

    DlRevF10/Dl[+] is an enhancer of photoreceptor cell R4 phenotype of fzhs.sev

    DlRevF10/Dl[+] is an enhancer of ommatidium phenotype of fzhs.sev

    DlRevF10/Dl[+] is an enhancer of ommatidium phenotype of dshhs.sev.B

    NOT Enhancer of
    Statement
    Reference

    DlRevF10/Dl[+] is a non-enhancer of ommatidium phenotype of Scer\GAL4hs.2sev, nmoUAS.cUa

    DlRevF10/Dl[+] is a non-enhancer of wing hair phenotype of Scer\GAL4en-e16E, kermitGS2053

    DlRevF10 is a non-enhancer of eye phenotype of upd1GMR.PB

    DlRevF10 is a non-enhancer of ommatidium phenotype of pkpk.sev

    Suppressor of
    NOT Suppressor of
    Statement
    Reference

    DlRevF10/Dl[+] is a non-suppressor of ommatidium phenotype of Scer\GAL4hs.2sev, nmoUAS.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 upd1GMR.PB

    DlRevF10 is a non-suppressor of ommatidium phenotype of pkpk.sev

    DlRevF10 is a non-suppressor of ommatidium phenotype of Scer\GAL4hs.2sev, pksple.UAS

    Other
    Statement
    Reference

    DlRevF10, Ser[+]/SerRX82, eygM3-12/eyg[+] has eye phenotype

    DlRevF10/Dl[+], Ser[+]/SerRX82, eygM3-12 has eye phenotype

    DlRevF10/Dl[+], SerRX82, eygM3-12/eyg[+] has eye phenotype

    DlRevF10, SerRX82 has scutum & macrochaeta phenotype

    Additional Comments
    Genetic Interactions
    Statement
    Reference

    DlRevF10, SerRX82 double mutant clones spanning the A1 fold in larval eye-antennal discs exhibit a failure of epithelial folding of the A1 fold.

    The formation of extra scutellar bristles observed in either Sirt12A-7-11/Sirt12A-7-11 or DlRevF10/+ single mutants is strongly enhanced in Sirt12A-7-11/Sirt12A-7-11;DlRevF10/+ double mutants, which on average have around seven scutellar bristles (instead of the four normally found in wild-type flies).

    The suppression of the WGMR.PG eye phenotype seen in eyes mosaic for cosH29 (generated using the ey-FLP/FRT system) is abrogated by heterozygosity for both DlRevF10 and SerRX82.

    The wing blistering phenotype seen in the posterior compartment of wings in flies expressing EogtGD5084 under the control of Scer\GAL4en.PU in the presence of Dcr-2Scer\UAS.cDa is dominantly partially suppressed if the flies are also heterozygous for DlRevF10.

    One copy of DlRevF10 enhances the small eye phenotype seen when Caf1-105NIG.12892R is expressed under the control of Scer\GAL4ey.PH.

    DlRevF10, SerRX106 double mutant clones in the adult thorax exhibit external sensory cell loss and an excess of neurons.

    A DlRevF10 SerRX106 double mutant background suppresses the extra socket cell phenotype seen in AP-47SHE-11 thorax clones, instead producing the external sensory cell loss and excess neurons seen in DlRevF10 SerRX106 double mutants.

    Wing disc clones mutant for DlRevF10 and SerRX106 give rise to clustered supernumerary sensory organ precursors (SOP), as all cells within the proneural field adopt the SOP fate. These are often spaced apart from each other, suggesting that a low level of lateral inhibition is still taking place.

    Expression of DlΔICD2.Scer\UAS.T:SV5\V5,T:Zzzz\His6 under the control of the ubiquitous driver Scer\GAL4mat.αTub67C.T:Hsim\VP16 restores N signalling in DlRevF10 SerRX106 mutant clones, leading to individualised sensory organ precursors. These are often spaced apart from each other, suggesting that a low level of lateral inhibition is still taking place.

    Expression of DlΔICD1.Scer\UAS.T:SV5\V5,T:Zzzz\His6 or DlΔICD1.ΔICD2.Scer\UAS.T:SV5\V5,T:Zzzz\His6 under the control of the ubiquitous driver Scer\GAL4mat.αTub67C.T:Hsim\VP16 fails to restore lateral inhibition by N signalling in DlRevF10 SerRX106 mutant clones. These are often spaced apart from each other, suggesting that a low level of lateral inhibition is still taking place.

    Expression of DlΔC.Scer\UAS.T:SV5\V5,T:Zzzz\His6 or DlK742R.Scer\UAS.T:SV5\V5,T:Zzzz\His6 under the control of the ubiquitous driver Scer\GAL4mat.αTub67C.T:Hsim\VP16 fails to restore lateral inhibition N signalling in DlRevF10 SerRX106 mutant clones.

    Expression of DlScer\UAS.T:Hsap\LDLR-int,T:Hsap\MYC under the control of the ubiquitous driver Scer\GAL4Scer\FRT.Rnor\CD2.Act5C does not rescue N-mediated lateral inhibition in DlRevF10 SerRX106 mutant clones, as a large number of adjacent sensory organ precursors are reproducibly detected.

    DlRevF10, SerRX106 double mutants display a strong neurogenic phenotype. The double mutant embryos display a large increase in total neuronal numbers.

    Heterozygous crb11A22 suppresses the DlRevF10/+ small eye phenotype. The suppression is achieved without altering the size of the facet lenses.

    Clones of cells doubly mutant for DlRevF10 and SerRX82 are found frequently in the wing disc at any stage of development and do not exhibit obvious phenotypic alterations.

    Clones of cells doubly mutant for DlRevF10 and SerRX82 and also expressing armS10.Scer\UAS.T:Hsap\MYC via Scer\GAL4αTub84B.PL (using the MARCM technique) remain integrated in the wing disc epithelium and do not exhibit growth defects.

    DlRevF10/+ enhances the wing vein thickening phenotype of dx152 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 dx152 hemizygotes or DlRevF10/+ animals. The double mutants show fusion of the ocelli in 37% of cases, compared to the 2% penetrance seen in dx152 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 DlRevF10 and Ras85DΔC40B 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 DlRevF10 clones.

    Co-overexpression of CycAScer\UAS.cWa, E2fScer\UAS.cNa and DpScer\UAS.cDa (using Scer\GAL4GMR.PF) does not significantly rescue the S phase phenotype seen in DlRevF10 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.

    Xenogenetic Interactions
    Statement
    Reference
    Complementation and Rescue Data
    Rescued by
    Not rescued by
    Comments

    Neurogenic phenotype, rescued by Dlm39.

    Images (0)
    Mutant
    Wild-type
    Stocks (1)
    Notes on Origin
    Discoverer

    Revertant.

    External Crossreferences and Linkouts ( 0 )
    Synonyms and Secondary IDs (15)
    Reported As
    Symbol Synonym
    DeltaRevF10
    Name Synonyms
    Secondary FlyBase IDs
    • FBal0044741
    References (109)