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General Information
Symbol
Dmel\dsh3
Species
D. melanogaster
Name
FlyBase ID
FBal0003140
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
dshV26, dshV6, l(1)V26, V26
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
deletion
Comment:
A deletion of 543 bases and insertion of one base that causes a frameshift after amino acid residue 94. The resulting sequence at the junction is ggtaacaatcTacggcgg.
Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference
Deletion of the open reading frame between nucleotides 496 and 1040, resulting in a frameshift after amino acid residue 94.
Deletion within the gene that removes, at least, part of the protein encoding domain.
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 ( 0 )
Disease
Interaction
References
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
embryonic leading edge cell & actin filament
embryonic leading edge cell & filopodium
embryonic leading edge cell & microtubule
macrochaeta & wing
wing & macrochaeta
wing & triple row | somatic clone
Detailed Description
Statement
Reference
dsh3/+ flies display wild-type hair patterns on the wing, thorax and eyes.
The induction of dsh3 clones in renal tubules leads to ectopic enteroendocrine-like cells (e.g. Pros-positive cells), as compared to controls.
Maternally and zygotically mutant dsh3 embryos (coming from mothers whose whole germline constitutes from dsh3 mutant cells only - created by the OvoD germline clone technique) show a segment polarity phenotype and no naked cuticle between denticle belts on the ventral epidermis (resulting in a lawn of denticles).
Heterozygous dsh3 mutant flies have normal wings.
All epidermal cells secrete denticles in embryos which are maternally and zygotically mutant for dsh.
Flies expressing dshY473F.T:Avic\GFP-EGFP in a dsh3 mutant background display strong PCP defects in all tissues analysed, including classical PCP defects in the thorax and wings, rough eyes with randomised chirality, symmetrical clusters and misrotation. Co-expression of dshY474F.T:Avic\GFP-EGFP does not enhance these phenotypes. Flies expressing dshY474F.T:Avic\GFP-EGFP in a dsh3 background display wild type PCP patterns in all tissues analysed.
dsh3 maternal/zygotic clones (expressing dshΔDIX.Scer\UAS under the control of Scer\GAL4arm.PS to remove the mild polarity defect of dsh3) display strong denticle alignment defects. Maternal dsh3 mutants (expressing dshΔDIX.Scer\UAS under the control of Scer\GAL4arm.PS to remove the mild polarity defect of dsh3) show a loss of denticles. dsh3 mutants display strong patterning defects, and all epidermal cells make denticle precursors. dsh3 maternal/zygotic mutant embryos show a ventral epidermis covered with denticles, and the naked regions of cuticle which separates the denticle belts in wild-type embryos are absent in these mutants. Every cell secretes a denticle, and denticle placement is not properly oriented toward the posterior of each cell. All ventral cells display a uniform square shape and lack normal alignment. dsh3 maternal effect mutants display wild-type cuticles.
Expression of dshDIX.Scer\UAS.T:ctail-arr in dsh3 mutants under the control of Scer\GAL4arm.PS produces embryos with completely naked cuticles.
Homozygous clones in the pupal wing (23 hours after puparium formation) do not affect polarity of trichomes in surrounding wild-type tissue.
In clones mutant for dsh3, the peripheral ommatidia do not undergo programmed cell death and so fail to release their associated 2o and 3o pigment cells to join the pigment rim. As a consequence, the pigment rim in dsh3 clones is significantly reduced in relation to neighbouring wild-type tissue.
Unlike neutral somatic clones, dsh3 homozygous somatic clones are rapidly lost from the somatic stem cell population of the germarium.
When clones are made in the eye disc ectopic dorsal furrows are induced.
The cuticles of embryos from dsh3 germline clones have an anterodorsal hole and are very short with most of the dorsal epidermis missing. At stage 13 in these embryos the leading edge cells fail to polarise or elongate dorso-ventrally.
Germband extension occurs normally in dsh3 homozygous embryos from mothers carrying dsh3 germ line clones. Polarisation of germband cells during germband extension also appears normal in these embryos.
Clones expressing dsh3 that are induced at the dorsal periphery of the eye show a loss of pigment rim tissue and an associated gain of extra ommatidia that extend almost to the head capsule. These extra ommatidia have a variable number of cells and many do not extend the depth of the retina. Some of these clones show an absence of dorsal rim ommatidia, while these are present in other clones.
Homozygous clones in the eye result in large clonal outgrowths. Additional rows of dorsal rim area ommatidia are seen in wild-type tissue adjacent to homozygous clones, probably due to overproliferation.
Homozygous clones generated at 72 hours after egg laying do not produce distal truncations of the leg, although leg polarity is abnormal.
During dorsal closure in dsh3 mutant embryos, frequent detachments of the amnioserosa from the epidermis occur. The leading edge cells lack filopodial activity, and have only a thin cable of actin, lacking distinguishable actin nucleation centers. In additions, these cells do not undergo D-V elongation or D-V polarization. One manifestation of this is that the microtubule bundles that form in these cells do not align perpendicular to the leading edge.
dsh1/dsh3 flies have planar polarity defects, resulting in an aberrant orientation of bristles and hairs.
Somatic clones of dsh3 in the eye produce long-range nonautonomous inversions of ommatidial polarity on their equatorial edge.
34% of ommatidia in homozygous mutant somatic clones in the eye are normal. 16.3% have rotated ommatidia, 38.3% have chirality defects, 11.3% are achiral (0% unscorable).
Has no effect on the eye phenotype produced by activated arm constructs. (either armS44Y.GMR or armS56F.GMR).
Embryos derived from homozygous female germline clones show defects in tracheal invagination, branch fusion and dorsal trunk formation.
Mutant embryos show shortening of the cuticle, fusion of denticle bands and absence the head skeleton and filzkorper.
Homozygous clones in polar regions of the eye show non-autonomous effects, with polarity inversion in tissue lying equatorial to the clone. Polarity errors are also seen within the clone. Clones elsewhere in the eye rarely show non-autonomous effects, but when they do, polarity inversions are seen on the equatorial side of the clone.
Clones in the eye-antennal disc that normally gives rise to head cuticle can cause ectopic ommatidia, ocelli or sensilla to develop.
Homozygous clones in the eye show an autonomous tissue polarity defect; ommatidia frequently show abnormal orientation and chirality.
Ommatidial orientations are disturbed, chiral shape is choosen randomly.
Large clones induced in the wing before 72hr AEL are associated with a notch in the wing margin. Small clones (induced after 72hr AEL) often leave the margin intact but fail to elaborate bristles.
Homozygous clones in the eye have interommatidial bristles.
When clones are induced in the wing disc, a second set of concentric folds forms in the disc epithelium, which may reflect the formation of a secondary proximo-distal axis. Mutant cells give rise to dorsal rather than ventral structures in the adult and can organize surrounding wild type cells to contribute to supernumerary legs, which branch out from the ventral surface of the normal leg.
Embryos derived from germline clones exhibit an extreme segment polarity phenotype in which naked cuticle and segmental furrows are replaced by a lawn of denticles. Head skeleton and filzkorpers fail to develop and the embryos fail to hatch.
In clones in the adult wing, ectopic bristles form off the wing margin in a wg-dosage-dependent fashion.
In homozygous embryos the second constriction is missing.
Only one central invagination fold of the stomodeal invagination is observed.
Embryos exhibit a lawn of denticle belts.
Sections of dsh1-dsh3 double mutant eyes show a disturbed ommatidial polarity within each ommatidium having the normal arrangement of photoreceptor cells.
Clones of cells in the wing display different phenotypes depending on the position of the clone within the wing blade. Cells within the wing blade show abnormalities in differentiation related to a function of dsh in tissue polarity. When clones reach the margin they behave as if they were in the middle of the wing blade, developing trichomes and non-pigmented cuticle. Cells outside these clones are induced to form ectopic bristles characteristic of the margin (this also occurs for arm clones. Clones of cells simultaneously mutant for both dsh and sgg do not produce a dsh mutant phenotype at the wing margin, but display the phenotype of cells mutant for sgg alone.
When both maternal and zygotic components of dsh are lacking, dsh embryos display patterning defects identical to those for wg null mutants such as wgl-17 : no segment borders form to define segments, the usual naked regions of cuticle are not seen and filzkorper and head structures are missing. The second midgut constriction fails to form. Clonal analysis reveals that dsh is required for patterning but not viability of ventral cells in the leg, with dsh clones producing supernumerary appendages from the ventral face. Wing clones show supernumerary cells in the triple row.
Clonal analysis revealed polarity defects in adult tissues as for dsh1, and that dsh is required autonomously for cell polarity. Similar mutant leg phenotypes, e.g. duplications and bifurcations, are produced by dsh clones, dsh, wg double heterozygotes and wg mutants. There is allele specificity in these interactions.
dsh3 embryos have a wg-like phenotype. In dsh3 embryos arm stripes could not be detected.
Females possessing homozygous germline clones when mated to wild type males produce two classes of embryos: heterozygous females are fertile and morphogenetically normal and hemizygous male embryos lack dorsal cuticle, posterior spiracles and filzkorper material. The ventral cuticle present has no naked cuticle in the thoracic or abdominal segments. Embryos show an aberrant pattern of cell death and lack of parasegmental and segmental boundaries.
larval lethal maternal-effect, partially rescuable by wild type sperm
External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
NOT Enhanced by
Suppressed by
NOT suppressed by
Enhancer of
NOT Enhancer of
Statement
Reference
dsh3/dsh[+] is a non-enhancer of visible phenotype of Scer\GAL4en-e16E, kermitGS2053
dsh3 is a non-enhancer of visible phenotype of RetMEN2B.GMR
dsh3 is a non-enhancer of visible phenotype of RetMEN2A.GMR
Suppressor of
Statement
Reference
NOT Suppressor of
Statement
Reference
Other
Phenotype Manifest In
NOT Enhanced by
Suppressed by
NOT suppressed by
Enhancer of
Statement
Reference
dsh3/dsh[+] is an enhancer of joint phenotype of ds1/ds05142
dsh3/dsh[+] is an enhancer of leg phenotype of ds1/ds05142
dsh3/dsh[+] is an enhancer of tarsal segment phenotype of ds1/ds05142
NOT Enhancer of
Statement
Reference
dsh3/dsh[+] is a non-enhancer of wing hair phenotype of Scer\GAL4en-e16E, kermitGS2053
dsh3 is a non-enhancer of eye phenotype of RetMEN2B.GMR
dsh3 is a non-enhancer of eye phenotype of RetMEN2A.GMR
dsh3 is a non-enhancer of ommatidium phenotype of Scer\GAL4hs.2sev, pksple.UAS
dsh3 is a non-enhancer of wing phenotype of Scer\GAL4bbg-C96, mamN.UAS
Suppressor of
Statement
Reference
dsh3/dsh[+] is a suppressor | partially of scutellum phenotype of Scer\GAL4pnr-MD237, hepUAS.cBa
dsh3/dsh[+] is a suppressor of ommatidium phenotype of Scer\GAL4hs.2sev, dcoUAS.cKa
dsh3/dsh[+] is a suppressor | partially of eye phenotype of CycEJP
dsh3 is a suppressor | partially of ommatidium phenotype of pkpk.sev
dsh3 is a suppressor of wing phenotype of Scer\GAL4en-e16E, armUAS.cWa
NOT Suppressor of
Statement
Reference
dsh3/dsh[+] is a non-suppressor of wing hair phenotype of Scer\GAL4en-e16E, kermitGS2053
dsh3 is a non-suppressor of eye phenotype of RetMEN2B.GMR
dsh3 is a non-suppressor of eye phenotype of RetMEN2A.GMR
dsh3 is a non-suppressor of ommatidium phenotype of Rac1V12.hs.sev
dsh3 is a non-suppressor of wing phenotype of Scer\GAL4bbg-C96, mamN.UAS
Other
Additional Comments
Genetic Interactions
Statement
Reference
Double-heterozygous flies of the genotype dsh[3]/+ together with either kmr1/+ or kmr2/+ display misoriented hair patterns on the wing, thorax and eyes, while single heterozygotes exhibit phenotypes similar to wild-type controls.
The segment polarity phenotype and the lack of naked cuticle between denticle belts, resulting in a lawn of denticles on the ventral epidermis, characteristic for maternally and zygotically mutant dsh3 embryos is not modified by Scer\GAL4arm.PU-driven expression of any of the following: sggScer\UAS.T:Myr-Src64B,T:Ivir\HA1, sggKK-MI.Scer\UAS.T:Myr-Src64B,T:Ivir\HA1, sggScer\UAS.T:Ivir\HA1 or sggKK-MI.Scer\UAS.T:Ivir\HA1.
In contrast to either mutation alone, flies heterozygous for Klp64Dk1 and dsh3 show loss of wing bristles and wing margin notching.
Expression of dshY473F.T:Avic\GFP-EGFP in a Abl2/+ mutant background partially rescues the lethality seen in dsh3. The PCP defects are not rescued.
dsh3 maternal/l(2)gl4 zygotic double mutants display a cuticle which resembles the l(2)gl4 maternal mutant phenotype. Patches of denticles are observed which lack proper alignment, and the ventral epithelium is continuous and formed. Denticle precursors are not properly oriented toward the posterior of cells and denticle placement appears to be random within each cell. dsh3 germ-line clones expressing armS56A.Scer\UAS.T:Zzzz\His6.T:Hsap\MYC under the control of Scer\GAL4arm.PS restores some pattern, but a strong denticle alignment phenotype remains. Embryos expressing armS56A.Scer\UAS.T:Zzzz\His6.T:Hsap\MYC under the control of Scer\GAL4arm.PS in a maternal dsh3 background display a complete absence of denticles.
dsh3 fz21/fz21 clones in the pupal wing (32 hours after puparium formation) cause neighbouring cells to point their trichomes towards the clone, as occurs with fz21/fz21 single mutant clones in the pupal wing. dsh3 Vangstbm-6/Vangstbm-6 clones in the pupal wing (32 hours after puparium formation) cause neighbouring cells to point their trichomes away from the clone, as occurs with Vangstbm-6/Vangstbm-6 single mutant clones in the pupal wing.
Expression of dcoScer\UAS.cKa under the control of Scer\GAL4hs.2sev in a dsh3/+ background completely suppresses the planar cell polarity and photoreceptor number phenotypes seen when dcoScer\UAS.cKa is expressed in a wild-type background.
The rapid loss of smo3 homozygous somatic clone cells from the somatic stem cell population of the germarium is significantly suppressed if the clone cells are also tkvQ199D.Scer\UAS; Scer\GAL4Act5C.PI (Scer\GAL80 method).
Unlike embryos from dsh3 germline clones, embryos from dsh3; sggM11 germ-line clones have no dorsal hole in their cuticles (although their dorsal cuticle is severely puckered), and have a dorso-ventrally polarised and extended leading edge at stage 13.
dsh3/+ enhances the severity of leg phenotypes in ds05142/ds1 animals: The length of the segments is reduced and most of the tarsal joints very reduced or completely absent.
The addition of dsh3 has no effect on the interneuron phenotype seen in drlScer\UAS.cCa, Scer\GAL4eg-Mz360 animals.
In crosses between nkd3/+, dsh3 flies and nkd3/+ flies, no enhancement or suppression of the dsh3 phenotype is seen.
Has no effect on the wing nicking phenotype seen in mamN.Scer\UAS, Scer\GAL4C96 flies.
Enhances wing margin phenotype of fzScer\UAS.N, Scer\GAL469B.
Embryos derived from homozygous doubly mutant germ lines, receiving neither maternal or zygotic wild type product, for sggM11 and dsh3 lack denticles on the ventral cuticle.
Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Rescued by
dsh3 is rescued by dshEGFP
Partially rescued by
dsh3 is partially rescued by dshEGFP
dsh3 is partially rescued by dsh1.EGFP
dsh3 is partially rescued by dshmut6.EGFP
dsh3 is partially rescued by dshY473F.EGFP
dsh3 is partially rescued by dshK417R.EGFP
dsh3 is partially rescued by dsh1.EGFP
dsh3 is partially rescued by dshKR.E.2x.GFP
dsh3 is partially rescued by dshST8.EGFP
dsh3 is partially rescued by dshΔQ
dsh3 is partially rescued by dshQ108
dsh3 is partially rescued by dsh1.tAa
dsh3 is partially rescued by dshΔEP+
dsh3 is partially rescued by dshΔDIX
Not rescued by
Comments
dshmut6.T:Avic\GFP-EGFP rescues the embryonic lethality of dsh3 animals. The resulting adults have largely wild-type wings and both leg bristles and wing hairs show normal planar polarisation. The rescued adults show a strong ectopic leg joint phenotype. dsh3 animals rescued to adulthood by dsh1.T:Avic\GFP-EGFP show a strong ectopic leg joint phenotype. Some dsh3 animals rescued to adulthood by dshT:Avic\GFP-EGFP show an ectopic leg joint phenotype.
Expression of dshT:Avic\GFP-EGFP fully rescues the lethality seen in dsh3 mutants. Expression of dshT:Zzzz\FLAG fully rescues the lethality and PCP defects seen in dsh3 mutants. Expression of dshT36A.T:Avic\GFP-EGFP fully rescues the lethality and PCP defects seen in dsh3. Expression of dshT252A.T:Avic\GFP-EGFP fully rescues the lethality and PCP defects seen in dsh3. Expression of dshS254A.T:Avic\GFP-EGFP fully rescues the lethality and PCP defects seen in dsh3. Expression of dshS266A.T:Avic\GFP-EGFP fully rescues the lethality and PCP defects seen in dsh3. Expression of dshS271A.T:Avic\GFP-EGFP fully rescues the lethality and PCP defects seen in dsh3. Expression of dshY280F.T:Avic\GFP-EGFP fully rescues the lethality and PCP defects seen in dsh3. Expression of dshS283A.T:Avic\GFP-EGFP fully rescues the lethality and PCP defects seen in dsh3. Expression of dshT314A.T:Avic\GFP-EGFP fully rescues the lethality and PCP defects seen in dsh3. Expression of dshT349A.T:Avic\GFP-EGFP fully rescues the lethality and PCP defects seen in dsh3. Expression of dshS406A.T:Avic\GFP-EGFP fully rescues the lethality and PCP defects seen in dsh3. Expression of dshT419A.T:Avic\GFP-EGFP fully rescues the lethality and PCP defects seen in dsh3. Expression of dshS451A.T:Avic\GFP-EGFP fully rescues the lethality and PCP defects seen in dsh3. Expression of dshT462A.T:Avic\GFP-EGFP fully rescues the lethality and PCP defects seen in dsh3. Expression of dshT467A.T:Avic\GFP-EGFP fully rescues the lethality and PCP defects seen in dsh3. Expression of dshS469A.T:Avic\GFP-EGFP fully rescues the lethality and PCP defects seen in dsh3. Expression of dshY474F.T:Avic\GFP-EGFP fully rescues the lethality and PCP defects seen in dsh3. Expression of dshS406E.T:Avic\GFP-EGFP fully rescues the lethality and PCP defects seen in dsh3. Expression of dshT419E.T:Avic\GFP-EGFP fully rescues the lethality and PCP defects seen in dsh3. Expression of dshS451E.T:Avic\GFP-EGFP fully rescues the lethality and PCP defects seen in dsh3. Expression of dshDEP6A.T:Avic\GFP-EGFP fully rescues the lethality and PCP defects seen in dsh3. Expression of dshC-term2.T:Avic\GFP-EGFP fully rescues the lethality and PCP defects seen in dsh3. Expression of dshC-term1-2.T:Avic\GFP-EGFP fully rescues the lethality and PCP defects seen in dsh3. Expression of dshC-term1-3.T:Avic\GFP-EGFP fully rescues the lethality and PCP defects seen in dsh3. Expression of dshC-term2-3.T:Avic\GFP-EGFP fully rescues the lethality and PCP defects seen in dsh3. Expression of dshC-term5Y-F.T:Avic\GFP-EGFP fully rescues the lethality and PCP defects seen in dsh3. Expression of dshΔC.T:Avic\GFP-EGFP fully rescues the lethality and PCP defects seen in dsh3. Expression of dsh1.T:Avic\GFP-EGFP partially rescues the lethality seen in dsh3. The PCP defects are not rescued. Expression of dshY473F.T:Avic\GFP-EGFP partially rescues the lethality seen in dsh3. The PCP defects are not rescued. Expression of dshK417R.T:Avic\GFP-EGFP partially rescues the lethality seen in dsh3. The PCP defects are not rescued.
Expression of dshST8.T:Avic\GFP-EGFP rescues the lethality of dsh3 mutants.
dshScer\UAS.cAa; Scer\GAL4da.G32 rescues the cuticles of embryos from dsh3 germline clones to normal length and suppresses the hole anterodorsal cuticle hole.
dshΔQ rescues the lethality of dsh3 flies, but a small fraction of the survivors have mild polarity and patterning defects. dshQ108 shows only 24% rescue of the lethality of dsh3 flies. The surviving adults have polarity and patterning defects including notched wings, disordered bristles and bifurcated legs.
dsh3 flies carrying dsh1.tAa are viable and have a dsh1 phenotype. Mutant embryos show shortening of the cuticle, fusion of denticle bands and absence the head skeleton and filzkorper. This phenotype is completely rescued by injection of dshcAa or dshΔbPDZ mRNA, partially rescued by injection of dshΔDIX or dshΔEP+ mRNA, and is not rescued by injection of dshΔDEP+, dshDIX, dshbPDZ or dshDEP+ mRNA.
Images (0)
Mutant
Wild-type
Stocks (4)
Notes on Origin
Discoverer
Comments
Comments
Maternal germline clonal analysis demonstrates a maternal effect, defects in segment polarity.
Mosaic analysis in the embryo revealed that the requirement for dsh product is cell autonomous.
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (11)
Reported As
Symbol Synonym
Name Synonyms
Secondary FlyBase IDs
    References (116)