A Database of Drosophila Genes & Genomes

FB2012_01, released January 20th, 2012
 

Allele Dmel\dsh3

General Information
SymbolDmel\dsh3SpeciesD. melanogaster
NameFlyBase IDFBal0003140
Feature typealleleAssociated geneDmel\dsh
Map ( GBrowse ) detailed view
Allele classloss of function allele, amorphic allele - genetic evidence
Mutagenethyl methanesulfonate
hide Recent Updates
Description
What does this section display?
This section contains items that were added to this record for each release. It currently only tracks new links between this FlyBase report and other FlyBase data classes (e.g. genes, references, stocks) or controlled vocabulary terms (e.g. GO, anatomy terms).
What does this section not display?
This section does not currently display links that were removed or gene model changes.
Update Feed
Click the icon below to subscribe to this FlyBase record and receive updates automatically through your feed reader.
FB2012_01
References
FB2011_10
All updates Click here to see a list of all updates to this record from FB2010_08 and on.
hide Nature of the Allele
Allele class
Mutagen
Mutations Mapped to the Genome
Type
Location
Additional Notes
References
deletion
evidence=experimental
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
DDBJ /
EMBL /
GenBank
DNA sequence
Protein sequence
Name
 
UniProtKB/Swiss-Prot
UniProtKB/TrEMBL
Progenitor genotype
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.
Cytology
hide Phenotypic Data
hide Phenotypic Class
hide 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
hide Detailed Description
Statement
Reference
dsh[3] maternal/zygotic clones (expressing dsh[ΔDIX.Scer\UAS] under the control of Scer\GAL4[arm.PS] to remove the mild polarity defect of dsh[3]) display strong denticle alignment defects. Maternal dsh[3] mutants (expressing dsh[ΔDIX.Scer\UAS] under the control of Scer\GAL4[arm.PS] to remove the mild polarity defect of dsh[3]) show a loss of denticles. dsh[3] mutants display strong patterning defects, and all epidermal cells make denticle precursors. dsh[3] 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. dsh[3] maternal effect mutants display wild-type cuticles.
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
 
hide External Data
Linkouts
hide Interactions
hide Phenotypic Class
hideSuppressed by
Statement
Reference
hideEnhancer of
Statement
Reference
hideNOT 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 RetMEN2A.GMR
dsh3 is a non-enhancer of visible phenotype of RetMEN2B.GMR
hideSuppressor of
Statement
Reference
dsh3/dsh[+] is a suppressor | partially of visible phenotype of CycEJP
hideNOT Suppressor of
Statement
Reference
dsh3/dsh[+] is a non-suppressor of visible phenotype of Scer\GAL4en-e16E, kermitGS2053
dsh3 is a non-suppressor of visible phenotype of RetMEN2A.GMR
dsh3 is a non-suppressor of visible phenotype of RetMEN2B.GMR
hide Phenotype Manifest In
hideNOT Enhanced by
Statement
Reference
dsh3 has phenotype, non-enhanceable by nkd3
hideSuppressed by
Statement
Reference
dsh3 has phenotype, suppressible | partially by Mmus\Dvl2fl.cKa
hideNOT suppressed by
Statement
Reference
dsh3 has phenotype, non-suppressible by nkd3
hideEnhancer 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
hideNOT 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 RetMEN2A.GMR
dsh3 is a non-enhancer of eye phenotype of RetMEN2B.GMR
dsh3 is a non-enhancer of wing phenotype of Scer\GAL4bbg-C96, mamN.Scer\UAS
hideSuppressor of
Statement
Reference
dsh3/dsh[+] is a suppressor | partially of eye phenotype of CycEJP
dsh3/dsh[+] is a suppressor of ommatidium phenotype of Scer\GAL4hs.2sev, dcoScer\UAS.cKa
dsh3 is a suppressor | partially of ommatidium phenotype of pkpk.sev
hideNOT 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 RetMEN2A.GMR
dsh3 is a non-suppressor of eye phenotype of RetMEN2B.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.Scer\UAS
hideOther
Statement
Reference
hide Additional Comments
hide Genetic Interactions
Statement
Reference
dsh[3] maternal/l(2)gl[4] zygotic double mutants display a cuticle which resembles the l(2)gl[4] 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. dsh[3] germ-line clones expressing arm[S56A.Scer\UAS.T:Zzzz\His6.T:Hsap\MYC] under the control of Scer\GAL4[arm.PS] restores some pattern, but a strong denticle alignment phenotype remains. Embryos expressing arm[S56A.Scer\UAS.T:Zzzz\His6.T:Hsap\MYC] under the control of Scer\GAL4[arm.PS] in a maternal dsh[3] background display a complete absence of denticles.
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.
hide Xenogenetic Interactions
Statement
Reference
hide Complementation & Rescue Data
Rescued by
Partially rescued by
dsh3 is partially rescued by dsh1.tAa
dsh3 is partially rescued by dshΔDIX
dsh3 is partially rescued by dshΔEP+
Not rescued by
dsh3 is not rescued by dshbPDZ
dsh3 is not rescued by dshDEP+
dsh3 is not rescued by dshDIX
Comments
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.
dshsevE.sevP.PS partially rescues the ommatidial polarity defects due to dsh3 somatic clones: ommatidia inside the clone have normal polarity, but ommatidia are inverted on the equatorial edge of the clone .
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.
hide Stocks ( 3 )
Bloomington
Kyoto
hide Notes on Origin
Discoverer
hide Comments
Mosaic analysis in the embryo revealed that the requirement for dsh product is cell autonomous.
Maternal germline clonal analysis demonstrates a maternal effect, defects in segment polarity.
hide External Crossreferences & Linkouts
Other Crossreferences
Linkouts
hide Synonyms & Secondary IDs ( 10 )
Reported As
Symbol Synonym
Name Synonym
Secondary FlyBase IDs
hide References ( 90 )
Generate a list of
List References by type
hide Recent research papers ( 3 )
McElwain et al., 2011, PLoS ONE 6(11): e26993
A suppressor/enhancer screen in Drosophila reveals a role for wnt-mediated lipid metabolism in primordial germ cell migration. [FBrf0216663]
Djiane and Mlodzik, 2010, PLoS ONE 5(6): e11228
The Drosophila GIPC homologue can modulate myosin based processes and planar cell polarity but is not essential for development. [FBrf0211141]
Kaplan and Tolwinski, 2010, J. Cell Sci. 123(18): 3157--3165
Spatially defined Dsh-Lgl interaction contributes to directional tissue morphogenesis. [FBrf0211705]
hide Recent reviews (0)
All reviews listed in FlyBase were published before 2010