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General Information
Symbol
Dmel\wgl-17
Species
D. melanogaster
Name
FlyBase ID
FBal0018509
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
wgCX4, wg1-17, wgCX4
Mutagen
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology

Polytene chromosomes normal.

Nature of the lesion
Statement
Reference

Point mutation caused by a small deletion removing the wg promoter.

Small deletion at the 5' end of the wg locus.

Deletion of 2.7kb removing the first exon.

Deletion in the 5' region of the wg gene.

2kb deletion around position 0 on the wg map.

deletion of 2 kb at 5' end of gene

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/larval dorsal vessel & embryonic myoblast

embryonic/larval somatic muscle & embryonic myoblast | dorsal

embryonic leading edge cell & actin filament

embryonic leading edge cell & filopodium

embryonic leading edge cell & microtubule

embryonic leading edge cell primordium & microtubule

larval hindgut & ectoderm

Detailed Description
Statement
Reference

wg1/wgl-17 larvae have significantly reduced bouton number and significantly increased bouton size at the neuromuscular junction of muscle 4, compared to controls.

wgl-17 homozygous embryos have severe morphological defects.

On average, wgl-17 clones induced in the wing disc in a wgKO;NRT-wg homozygous background are smaller than wgl-17 clones induced in the wing disc in a wild-type background.

Mutant embryos have a "lawn of denticles" phenotype, lacking the naked cuticle that normally separates the eight abdominal segments. The denticles are large and strongly hooked, with the direction of the hook alternating between anterior and posterior in a segmentally repeating pattern.

The anterior dorsocentral bristle is missing in 61% of wgSp-1/wgl-17 flies. When present, it is 14% shorter than normal.

The cardiogenic mesoderm is absent in stage 12 mutant embryos.

wgl-17/wgl-12 embryos show a loss of neurons derived from SOPs in the posterior of the parasegment: the vbd neuron is lost in 100%, the class III lost in 85% and class II neurons in 73% of parasegments. Both class IV neurons, vdaB and v'ada, always form. Multidendritic neuron loss in wgl-17/wgl-12 mutants is always preceded by the loss of posterior SOPs: all four SOPs are lost in 45%, three are lost in 35%, and two lost in 20% of parasegments.

wgl-12/wgl-17 mid-pupal stage flies switched to the non-permissive temperature exhibit less cell death and a higher interommatidial precursor cell (IPC) number per hexagon than flies maintained at the permissive temperature.

wgl-17 retinal clones 28 hours after puparium formation display reduced cell death compared to controls.

There are abnormalities in the shape, organisation and number of cone cells in wgl-17 retinal clones 42 hours after pupal formation. This phenotype is seen throughout the eye epithelium.

wgl-17 clones in the eye discs of third instar larvae have fewer cone cells than controls.

wgl-17 clones in photoreceptors are sufficient to cause defects in cone cell specification at both the third instar larval and pupal stages. No cone cell defects are seen when clones are induced only in the cone cells or the interommatidial cells.

wgl-17 mutants exhibit defects in para-segmental boundary interfaces.

The posterior compartment of wings composed of mainly homozygous wgl-17 mutant cells (in a "Minute" background) are reduced in size compared with control wild-type posterior compartments. This correlates with with the loss of a substantial portion of the posterior tissue in imaginal wing discs.

Mutants lack the eve-positive RP2 lineage.

~70% of hemisegments in mutant embryos are missing one or more row 5 neuroblasts (NBs), such as NB5-4 (which is affected the most), NB5-5 and NB5-2.

wg1/wgl-17 mutants display a wing-to-notum transformation.

Cell proliferation (assayed through BrdU incorporation) is not observed in the PNS region of wgl-17 homozygous embryos. Proliferation can be seen in wgl-17 heterozygotes. Proliferation is also observed in the head and ventral CNS.

The RNA-null wgl-17 mutant produces a 'lawn of denticles' phenotype.

The maxillary segments of wgl-12/wgl-17 mutant embryos are smaller than those of wild-type embryos.

Mutant embryos show a "lawn of denticles" cuticle phenotype.

In wgl-17 mutants, midline cells do not differentiate and instead die during late embryogenesis.

Cells within the leg primordia of wgl-17 mutant embryos begin a process of invagination that is characteristic of tracheal cells.

Stage 15 wgl-17 embryos have only 14 genital disc precursor cells, instead of the wild-type number of 15.

Mutant embryos exhibit a complete loss of cI and cII cluster of slou expressing muscle founder cells.

wgl-17 embryos lack the slou-expressing cluster I and II founder cells and have no RP2 neurons. wgl-17 larvae lack naked cuticle and proper denticle diversity.

No posterior spiracles are present in wgl-17 larvae.

Around 30% of wgl-17/+ first instar larvae have cuticular segmentation defects.

wgl-12/wgl-17 animals raised at 18oC until 28 hours after puparium formation (developmentally equivalent to approximately 17 hours APF at 25oC) and then shifted to 25oC for 7 hours show a small but significant decrease in cell death in the pupal retina. Homozygous clones in the eye disc result in a decrease in the amount of cell death in eye discs assayed at 20 hours after puparium formation.

The corpus cardiacum is normal in size in mutant embryos, but shows defects in migration.

In stage-15 wgl-17 mutant embryos, the lymph gland, cardioblasts and pericardial nephrocytes fails to develop from the cardiogenic mesoderm.

Instead of being elongated in a dorsal-ventral direction, embryonic leading edge cells in stage 13 wgl-17 homozygous embryos are stretched in an anterior-posterior direction. Only the posterior dorsal closure zipper is initiated in these embryos.

The areas of naked cuticle are replaced by denticles in the mutant embryos, resulting in a "lawn of denticles" without clear polarity.

Mutant embryos have a reduced number of visceral mesoderm parasegmental cells.

Mutant animals exhibit separated nerve roots and dendritic fields in the embryonic motor system, as in wild type.

In homozygous mutant germ-line clones, The alternation of naked cuticle and denticle belts seen in wild-type is replaced by a continuous lawn of denticles.

The cuticles of wgl-17/wgl-17 mutant embryos lack of smooth cuticle.

The cuticles of mutant embryos have reduced bands of naked cells, though they are not totally lost and the number of denticles is increased. This is due to an increase in numbers of denticle types 2,3 and 4.

wgspd-fg:Sp-1/wgl-17 animals have a severely atrophied wing with no margin. The alula of the proximal wing is missing.

wgl-17 clones at the edge of the eye are identical to wild type.

wgl-16/wgl-17 wing discs raised at 18oC show a double notum phenotype.

Dorsal closure is much slower and more disorganized in wgl-17 mutant embryos than in wild-type. The leading edge cells lack filopodial activity, and have only a thin cable of actin, lacking distinguishable actin nucleation centers. This cable does not look contractile in time-lapse movies. In these mutants, the leading edge 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.

wgl-12/wgl-17 animals upshifted to the restrictive temperature during the late second or early third instar develop into pharate adults with hinge defects that consistently show reductions of axillary sclerite 3. Homozygous clones do not cause wing hinge phenotypes.

Neuroblast NB 7-3 is missing in 75% of mutant hemisegments.

Visceral mesoderm is expanded in mutant embryos.

The wgl-16/wgl-17 combination results in pharate adults with wing to notum transformations and loss of halteres. Loss of antennae and dorsalisation of leg structures is also seen. Wing discs show replacement of the wing blade by a mirror duplication of the notum in these animals. wgl-12/wgl-17 wing discs shifted to the restrictive temperature for 24 hours at the beginning of the second larval instar show a profound wing to notum transformation.

wgl-16/wgl-17 genital discs are smaller than wild type.

In wgl-17 mutants some dorsal trunk is still formed.

Hindgut visceral mesoderm does not differentiate. Hindgut ectoderm is small, due to failure of division of proctodeal cells after gastrulation.

The naked regions between denticle belts are deleted and the length of the cuticle is greatly reduced in mutant embryos.

wgl-12/wgl-17 embryos raised at the restrictive temperature from 8 hours of development show a reduction in the number of 4o denticle rows from 8-9 to 4-5 in the dorsal epidermis of the embryo. The anterior half of the parasegment is unaffected (an expansion of 3o denticles is never seen).

The mesodermal P2 progenitor is missing in mutant embryos.

Heart and dorsal muscle progenitors do not form.

No lateral trunk fusion is seen in the tracheal system in mutant embryos, but some fragments of dorsal trunk are formed and often fuse, even though the embryo and the tracheae are generally malformed. Defects in tracheal invagination, branch fusion and loss of dorsal branches are seen.

The gnathal lobes are reduced in mutant embryos.

Cell division fails in the Malpighian tubule primordia of mutant embryos, producing tubules of very reduced size. In these tiny tubules no tip cells develop.

wg1/wgl-17 flies exhibit ectopic notum and have no wings.

Different types of ordered denticle types, particularly types 4 and 5 can be seen in mutant embryos.

Mesoderm migration is normal in mutant embryos. Embryos develop an extensive tracheal network which has an abnormal pattern due to the associated segmentation defect. Expression of bnlScer\UAS.cSa under the control of Scer\GAL469B in these embryos leads to an overproduction of fine tracheal branches, much as occurs when bnlScer\UAS.cSa is ectopically expressed in a wild-type background.

Mutant embryos show a lawn of uniform denticles.

Homozygous clones in the wing disc have no effect on the shape of the dorsal/ventral boundary.

wgl-17 transforms the whole ventral epidermis towards the denticle fate.

Embryonic cuticle is covered with denticles and lacks intervening naked cuticle.

The eve-positive GMC-1 -> RP2/sib lineage is missing in wgl-17 embryos.

Formation of the visceral mesoderm is normal in homozygous embryos, and the visceral mesoderm migrates to cover the gut and form midgut constrictions.

Homozygous embryos secrete no ventral naked cuticle and instead produce denticles consisting primarily of a single morphology which resembles the large denticles found in the fifth row of the wild-type denticle belt. Segmental pattern in the dorsal cuticle is abolished and the dorsal expanse is greatly reduced. wgDE/wgl-17 embryos show all 6 denticle types, separated by small expanses of naked cuticle. These embryos show segmentally repeating dorsal cuticle structures, with a slightly abnormal arrangement.

The lawn of denticles phenotype of wgl-17 embryos is replaced by naked cuticle if the embryos are also expressing tshScer\UAS.cGa under the control of Scer\GAL469B.

Homozygous embryos show severe disruptions in head formation. The antennal sense organ is frequently duplicated.

wgl-16/wgl-17 is a strong hypomorphic combination that causes a wing to notum transformation in 92% of flies.

Does not affect the polarity reversal phenotype produced by sggM11 clones in the eye.

Double mutant phenotype with CrebA mutants is additive.

Transheterozygotes with wgSp-1 exhibit occasional etching of the wing margin and hold their wings in an abnormal out-stretched position.

wgl-16/wgl-17 mutant clones cause a phenotype in the external male genitalia; a reduction in number of clasper teeth, two lateral plates are fused to one with reduced number of bristles and there is rudimentary penis apparatus. Internal male and female genitalia are completely deleted. External female genitalia is generally normal.

Homozygous mutants lack RP2 and RP2 sibling neurons. Double mutants with gsb525 exhibit duplicated RP2 and RP2 sibling neurons.

25% of wgl-17/wgP flies have wings on the prothoracic segment, and the mesothoracic wings and metathoracic halteres are always absent.

Embryos show little denticle diversity and secrete no naked cuticle. Expression of wgPE2.hs.T:Ivir\HA1 or wgPE2.hs by three consecutive heat shocks in wgl-17 embryos restores denticle diversity, but there is no secretion of naked cuticle. Expression of wgPE2.hs.T:Ivir\HA1 or wgPE2.hs using a single heat shock at 6 hours of development in wgl-17 embryos produces reorientation of the denticles toward the ventral midline, but no specification of naked cuticle. Expression of wgPE2.Scer\UAS.T:Ivir\HA1 or wgPE2.Scer\UAS using Scer\GAL4e22c in wgl-17 embryos restores denticle diversity, but there is no specification of naked cuticle along the ventral midline. Expression of wgPE4.hs.T:Ivir\HA1, wgPE4.hs, wghs.T:Ivir\HA1 or wghs.PH by three consecutive heat shocks in wgl-17 embryos restores denticle diversity and naked cuticle. Expression of wghs.T:Ivir\HA1 or wghs.PH using a single heat shock at 6 hours of development in wgl-17 embryos produces specification of naked cuticle along the ventral midline, but little denticle diversity. The denticles are reoriented toward the ventral midline. Expression of wgScer\UAS.cHa, wgScer\UAS.cHa.T:Ivir\HA1, wgPE4.Scer\UAS.T:Ivir\HA1 or wgPE4.Scer\UAS using Scer\GAL4e22c in wgl-17 embryos causes all ventral epidermal cells to secrete naked cuticle.

wgspd-fg:Sp-1/wgl-17 flies have a substantial loss of wing tissue, and structures distal to the posterior cross vein are missing.

Clones in the adult abdomen that are doubly mutant for Pka-C1E95 and wgl-17, or triply mutant for Pka-C1E95, wgl-17 and dppunspecified have the same phenotype as single mutant Pka-C1E95 clones.

Homozygous larvae have a lawn of denticles, almost exclusively of the row 5 type, with no interspersed naked cuticle.

Stage 11 embryos exhibit normal segmental organisation of the dorsal median cells.

Segments shows a mirror image duplication of the denticle belts at the expense of naked cuticle so that a continuous sheet of denticle is produced. Embryos lack head structures and filzkorper. Dorsally many myoblasts remain unfused and no segment identities can be assigned. Ventrally the structure and appearance of attachments seems quite normal though the number of apodemes is reduced roughly to half. Structure of myotubes is severely disturbed.

Clones in the eye lack interommatidial bristles.

Homozygous clones induced in first instar larvae produce abnormalities in the ventral side of the leg. Pattern elements from the ventral side are missing, and may or may not be replaced with a duplicate version of the remaining dorsal part of the leg. Duplications are arranged as mirror images. Leg truncations are also seen. Homozygous clones doubly mutant for dppd12 and wgl-17 show defects in both the ventral and dorsal sides of the leg. The frequency of duplications is reduced compared to the single mutant homozygous dppd12 or wgl-17 clones.

ctL32; su(Hw)e2 flies heterozygous for wgl-17 display a weak ct wing phenotype.

wgl-17/wgspd-fg flies show a milder version of the hinge phenotype seen in wgspd-fg homozygotes. Milder phenotype is thought to be due to transvection. Heterozygotes with wgspd-fg are embryonic lethal.

wgl-17/wgSp-1 flies are viable and exhibit loss of anterior dorsocentrals and loss of microbristles located in the wg-expression domain of the notum. Individuals in combination with wgP and wgl-16 are pupal lethal, and in combination with wgspd-j2 are embryonic lethal. Individuals are adult viable and exhibit the wing phenotype when in combination with wg1. When in combination with wgSp-revP individuals are pupal lethal, pharate escapers lack antennae, legs and anterior dorsocentrals.

Dorsolateral ectoderm of the embryo shows a transformation towards tracheal cells but most of them do not invaginate. Some dorsal trunk forms.

In homozygous embryos the second constriction is missing.

Embryos give rise to abnormally short larvae which form a lawn of ventral denticles.

Complete loss of naked cuticle but vestiges of polarity remain visible.

Abnormally patterned muscle fibres form dorsally and ventrally, but laterally only myosin expressing cells are detected. Heart is absent and the gut has grossly abnormal morphology. Loss of slou expression normally seen in wgl-17 mutants is rescued by Scer\GAL4 line 69B acting on P{UAS(-FRT)wg.ts}, slou-expressing cells are in the appropriately positioned clusters and the epidermis phenotype is substantially rescued. wg expression in the mesoderm, driven by P{GAL4-twi.B} expression, is capable of restoring some ectodermal en expression as well as partially rescuing the cuticle mutant phenotype.

Clones that cross the wing dorsal/ventral boundary can cause extensive non-autonomous loss of wing tissue. Clones restricted to one side do not cause nicking of the wing.

Coordinate mutant.

Embryos exhibit variability in the pattern of NB 5-2.

Surviving cells of the embryonic dorsal cuticle form a lawn of fine hairs of the 4o cell type. When en is restored in dorsal patches using enhs.P, all cells show altered identities even though en is only expressed in a subset. 1o, 2o and 3o cell types are all restored.

When newly hatched wgl-12/wgl-17 larvae are shifted to a non-permissive temperature the normal crescent-shaped neuropil of the medulla, the target for retinal axons R7 and R8, collapsed into a small circular remnant. The number of developing ommatidia is reduced. Later inactivations of wg produce less severe reductions in the number of developing ommatidia, the size of the lamina and the size of the medulla neuropil. In all cases the reduction of the structures is from their dorsal and ventral extents. The number of outer proliferative center cells incorporating BrdU is markedly decreased in the Fas2 expressing domain of wg and dpp early third instar brains.

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.

The cuticle of double mutant wghs.PN, wgl-17 embryos shows an embryo of almost wild type size with partially restored head and tail structures (filzkorper) and a segmental denticle pattern.

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. A small fraction of wgP/wgl-17 pharate adults have misoriented bristles on the notum, head and abdomen.

Mutant embryos have a lawn of row-5-type ventral denticles, with segmental polarity reversals.

The sensory mother cells of the posterior postalar, and the anterior and posterior dorsocentral and scutellar sense organs are absent from wgl-12/wgl-17 discs.

Segmental boundaries normally found in the embryonic epidermis are absent in homozygotes.

Instead of usual four, only get two Malpighian tubule primordia in the embryo. These eventually elongate to produce two rudimentary tubules, that go on to produce uric acid. BrdU labelling indicates that the cells in the primordia are not replicating their DNA. Expression of stg in proctodeum is absent.

lab expression in midgut (as indicated by lab-lacZ fusion genes) reduced but extended posteriorly as far as the third midgut constriction, though effects likely to be indirect.

Cuticle ventral pattern resembles that of wg individuals: abdominal segments are covered in denticles.

Does not interact with RpII140wimp maternal effect.

After stage 11 most ptc transcripts begin to disappear and by the end of germ band retraction ptc is absent from most of the cells.

lab and abd-A expression is not altered in wgl-17 mutant embryos. wgl-17 homozygotes lack the second midgut constriction.

wgl-8 and wgl-17 embryos show no localized increases of arm protein in the epidermis at the time the stripes would be apparent in wild type embryos, but increases were seen in domains that do not express wg.

wg mutant embryos lack all Keilin's organs. wgL4/wgl-17 embryos grew in in vivo culture, but produced rather small implants containing larval gut, salivary gland, fat body and occasionally Malpighian tubules, but lacked imaginal disc material. Metamorphosed implants were necrotic and none had recognisable adult cuticular structures.

embryonic lethal

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

wg[+]/wgl-17 is a suppressor of increased cell number | female | adult stage | heat sensitive phenotype of Df(2R)BSC132/Mmp2Y53N

wg[+]/wgl-17 is a suppressor | partially of size defective | adult stage phenotype of Nspl-1

wg[+]/wgl-17 is a suppressor | partially of visible phenotype of CycEJP

wg[+]/wgl-17 is a suppressor of visible phenotype of Scer\GAL4en-e16E, armUAS.cWa

wgl-17 is a suppressor of visible phenotype of Scer\GAL469B, fzUAS.N

NOT Suppressor of
Other
Phenotype Manifest In
Enhanced by
NOT Enhanced by
Statement
Reference

wgl-17 has wing phenotype, non-enhanceable by Atg4bP0997/Atg4bP0997

wgl-17 has phenotype, non-enhanceable by fz2UAS.cZa/Scer\GAL4e22c

wgl-17 has phenotype, non-enhanceable by Nipped-A323

wgl-17 has phenotype, non-enhanceable by Nipped-B292.1

wgl-17 has phenotype, non-enhanceable by Nipped-B407

wgl-17 has phenotype, non-enhanceable by RpL3845-72

wgl-17 has phenotype, non-enhanceable by Nipped-A222.3

wgl-17 has phenotype, non-enhanceable by Nipped-A2

Suppressed by
Statement
Reference

wgl-17 has denticle phenotype, suppressible | partially by SoxNNC14

wgl-17 has denticle phenotype, suppressible | partially by pan2

wg1/wgl-17 has wing phenotype, suppressible by HipkUAS.Tag:HA/Scer\GAL469B

wgl-17 has denticle belt phenotype, suppressible | partially by SoxNNC14

wgl-17 has denticle | ectopic phenotype, suppressible by SoxNU6-35

wgl-17 has embryonic leading edge cell primordium & microtubule phenotype, suppressible by armS10.UAS.Tag:MYC/Scer\GAL4da.G32

wgl-17 has RP2sib neuron phenotype, suppressible by slp1hs.PC

wgl-17 has neuroblast NB4-2 phenotype, suppressible by slp1hs.PC

wgl-17 has RP2 motor neuron phenotype, suppressible by slp1hs.PC

wgl-17 has RP2 motor neuron phenotype, suppressible by slp2hs.PC

wgl-17/Df(2L)DE has phenotype, suppressible | partially by dallyhs.PJ

wgl-17 has denticle phenotype, suppressible by Apc2ΔS

wgl-17 has embryonic epidermis phenotype, suppressible by ovosvb-2

wgl-17 has denticle belt phenotype, suppressible by ovosvb-2

wg1/wgl-17 has wing phenotype, suppressible by fz3G10

wgl-17 has embryonic epidermis phenotype, suppressible by pan3

wgl-17 has denticle belt phenotype, suppressible by pan3

wgl-17 has denticle belt phenotype, suppressible by Df(3R)Espl22

NOT suppressed by
Statement
Reference

wgl-17 has embryonic leading edge cell primordium & microtubule phenotype, non-suppressible by armS10.UAS.Tag:MYC/Scer\GAL4332.3

wgl-17 has wing phenotype, non-suppressible by Atg4bP0997/Atg4bP0997

wgl-17 has phenotype, non-suppressible by Wnt4UAS.cGa/Scer\GAL4da.G32

wgl-17 has embryonic/larval somatic muscle & embryonic myoblast | dorsal phenotype, non-suppressible by Scer\GAL4twi.PG/slp1UAS.cSa

wgl-17 has embryonic/larval dorsal vessel & embryonic myoblast phenotype, non-suppressible by Scer\GAL4twi.PG/slp1UAS.cSa

wgl-17 has phenotype, non-suppressible by fz2UAS.cZa/Scer\GAL4e22c

wgl-17 has phenotype, non-suppressible by dallyhs.PJ

wgl-17 has denticle phenotype, non-suppressible by Scer\GAL4arm.PS/EgfrDN.UAS

wgl-17 has denticle phenotype, non-suppressible by Egfrf1

Enhancer of
NOT Enhancer of
Statement
Reference
Suppressor of
Statement
Reference

wg[+]/wgl-17 is a suppressor of interfollicle cell | supernumerary | heat sensitive phenotype of Df(2R)BSC132/Mmp2Y53N

wg[+]/wgl-17 is a suppressor | partially of eye phenotype of Nspl-1

wg[+]/wgl-17 is a suppressor | partially of cone cell phenotype of Nspl-1

wg[+]/wgl-17 is a suppressor | partially of photoreceptor phenotype of Nspl-1

wg[+]/wgl-17 is a suppressor | partially of denticle belt phenotype of nkd2

wgl-17 is a suppressor of arista | supernumerary phenotype of obk1

wg[+]/wgl-17 is a suppressor | partially of eye phenotype of CycEJP

wg[+]/wgl-17 is a suppressor of wing | posterior phenotype of Scer\GAL4en-e16E, armUAS.cWa

wg[+]/wgl-17 is a suppressor of genitalia phenotype of dallygem/dally06464

wgl-17 is a suppressor | partially of leg | somatic clone phenotype of Pka-C1H2

NOT Suppressor of
Statement
Reference

wgl-17 is a non-suppressor of genital disc phenotype of ix1

wgl-17 is a non-suppressor of denticle belt phenotype of AxnS044230

wgl-17 is a non-suppressor of ommatidium phenotype of Rac1V12.hs.sev

wgl-17 is a non-suppressor of phenotype of dshhs.sev.B

Other
Statement
Reference
Additional Comments
Genetic Interactions
Statement
Reference

The highly prevalent duplication of mesanotum structures observed upon the expression of domeKK104700 under the control of Scer\GAL4sd.PU is slightly enhanced by wgl-17 heterozygosity (and Dicer-2, for more efficient RNAi).

The increase in average cell number in the stalks between egg chambers which is seen in Mmp2Y53N/Df(2R)BSC132 and in Mmp2Y675N/Df(2R)BSC132 females after being shifted to the restrictive temperature is dominantly suppressed if the females also carry a single copy of wgl-17.

The wgl-17 denticle phenotype is modified in combination with any of ckAN9, ckCB16, ckKT9, ckPS10, ckPT14, ckPJ17 or ck7, such that the double mutants have denticles with a rounded appearance and no distinctive hook.

pan2 partially suppresses the wgl-17 denticle phenotype: denticle diversity is restored but not naked cuticle.

In wgl-17 ckKT9 ; pan2 triple mutants, smaller anterior denticles can have sharp points, while larger posterior denticles remain rounded and some appear fragmented.

SoxNNC14 partially suppresses the wgl-17 denticle phenotype: some segmentation is restored to the pattern, without increasing denticle diversity.

wgl-17 ckKT9 SoxNNC14 triple mutant embryos show a dramatic reduction in denticle size and many of the denticles are fragmented into one or two short projections. Actin bundles in the epidermal cells are split into two or sometimes three separate aggregates.

wgl-17/+ ; lqfR03685/lqfRΔ117 adult escapers have severely defective eyes, ranging from kidney-shaped to nearly absent. They also have defects in the head cuticle.

Expression of pnrSA.Scer\UAS.β under the control of Scer\GAL4pnr-MD237 results in greater rescue of the loss of dorsocentral bristles seen in wgSp-1/wgl-17 flies than expression of pnrScer\UAS.β under the control of Scer\GAL4pnr-MD237.

Expression of scSA.Scer\UAS under the control of Scer\GAL4DC results in greater rescue of the loss of dorsocentral bristles seen in wgSp-1/wgl-17 flies than expression of scScer\UAS.cUa under the control of Scer\GAL4DC.

wgl-17/+ suppresses the necrosis seen in adult eyes when NGD144 is driven by Scer\GAL4sev.PU.

wgl-17/+ suppresses the cone cell loss phenotype seen in the third instar eye discs when NGD144 is driven by Scer\GAL4sev.PU.

Nspl-1 with one copy of wgl-17 suppresses the adult eye size phenotype seen in Nspl-1 mutants.

Nspl-1 with one copy of wgl-17 suppresses the cone cell and photoreceptor loss phenotypes seen in Nspl-1 third instar larvae.

The leading edge cell in the anterior compartment just anterior to the parasegment boundary is transformed into an ectopic mixer cell in wgl-17 embryos expressing armS10.Scer\UAS.T:Hsap\MYC under the control of Scer\GAL4en-e16E assayed by marker expression (in the abdominal segments of wild-type embryos at the end of dorsal closure, the "mixer cell" moves across the segment boundary from the anterior compartment to the posterior compartment, but the cell in the equivalent position relative to the parasegment boundary does not show this "mixing" behaviour).

Scer\GAL4prd.RG1>dshScer\UAS.cAa-overexpressing embryos are readily identifiable amongst wgl-17 homozygotes by their four wide naked zones interspersed between their denticle bands.

The ectopic RP2 neuron seen in midlos1 mutants is missing in 75-96% of the hemisegments in midlos1, wgl-17 double mutants.

Expression of hipkScer\UAS.T:Ivir\HA1 under the control of Scer\GAL469B in a wg1/wgl-17 mutant background results in proper wing development and rescues the wing-to-notum transformation.

The RNA-null wgl-17 mutant 'lawn of denticles' phenotype is partially suppressed by SoxNNC14.

wgl-17; SoxNU6-35 double mutant embryos have cuticles with few or no ectopic denticles.

Stage 15 ptc9 wgl-17 double mutant embryos have the same number of genital disc precursor cells as wgl-17 single mutants. This is a reduction compared to wild type, and a huge reduction compared to ptc9 single mutant embryos.

Expression of Nrt::wgScer\FRT-.Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4wg.PM rescues the slou expressing founder cell phenotype in wgl-17 embryos. In fact, there is an expansion of slou cluster II in 57% of hemisegments examined, indicating that the mesoderm is experiencing increased wg signalling.

The excess naked cuticle phenotype seen in nkd2 embryos is partially suppressed by wgl-17/+. The ability of wgl-17/+ to suppress the excess naked cuticle phenotype of nkd2 embryos is suppressed by RacGAP50CAR2 or RacGAP50CDH15; the triple mutant embryos secrete uniform cuticle with no denticle belts. Expression of nkdScer\UAS.cZa under the control of Scer\GAL4e22c in a wgl-17/+ background results in fusions between denticle belts due to loss of intervening naked cuticle. This effect is suppressed if the embryos are also heterozygous for RacGAP50CAR2; the triple mutant embryos have a wild-type cuticle pattern.

Wnt4K2/wgl-17 flies show no detectable eye defects.

The frequency of cuticular segmentation phenotypes in wgl-17/+ first instar larvae is not significantly changed in animals with a egl3e/egl1 mutant mother.

armS10.Scer\UAS.T:Hsap\MYC; Scer\GAL4da.G32 suppresses the transformation of naked ventral cuticle to denticles in wgl-17 homozygous embryos. Many of the resulting embryos have the armS10.Scer\UAS.T:Hsap\MYC; Scer\GAL4da.G32 overexpression phenotype of a completely naked ventral cuticle. armS10.Scer\UAS.T:Hsap\MYC; Scer\GAL4da.G32 suppresses the dorsal-ventral elongation and orientation of microtubule bundles in the leading edge cells of stage 13 wgl-17 homozygous embryos. armS10.Scer\UAS.T:Hsap\MYC; Scer\GAL4332.3 completely fails to suppress these phenotypes. dshScer\UAS.cAa; Scer\GAL4da.G32 partially suppresses he transformation of naked ventral cuticle to denticles and the shortening of the cuticle seen in wgl-17 homozygous embryos. The dorsal side of these cuticles have some 'warts'. dshScer\UAS.cAa; Scer\GAL4da.G32 suppresses the loss of dorsal ventral polarity in the leading edge cells of stage 13 wgl-17 homozygous embryos, but only weakly rescues elongation of these cells. dshΔDEP+.Scer\UAS; Scer\GAL4da.G32 partially suppresses the transformation of naked ventral cuticle into denticles and reduction in cuticle length seen in cuticles from wgl-17 homozygous embryos, and an completely suppress the dorsal hole in these cuticles. dshΔDEP+.Scer\UAS; Scer\GAL4da.G32 suppresses, the loss of dorsal ventral polarity in the leading edge cells of stage 13 wgl-17 homozygous embryos but fails to rescue elongation of these cells. However, initiation of the anterior zipper during dorsal closure is rescued. dshΔDIX.Scer\UAS; Scer\GAL4da.G32 does not suppress the transformation of naked ventral cuticle into denticles in cuticles from wgl-17 homozygous embryos. The resulting cuticles are even shorter and more puckered than those from wgl-17 homozygous embryos, have an enlarged dorsal hole.

hhScer\UAS.cIa; Scer\GAL4prd.RG1 fails to rescue metameric furrow formation in Df(2R)enE; wgl-17 double homozygous embryos. enScer\UAS.cGa; Scer\GAL4prd.RG1 rescues metameric furrow formation in Df(2R)enE; wgl-17 double homozygous embryos, but these furrows disappear prematurely (before stage 13) on the ventral side of the embryo. Failure of metameric furrow formation in armS10.Scer\UAS.T:Hsap\MYC; Scer\GAL4en-e16E embryos homozygous for hhAC is not suppressed by wgl-17/wgl-17. In stage 13+ armS10.Scer\UAS.T:Hsap\MYC; Scer\GAL4en-e16E embryos homozygous for wgl-17, the metameric furrows are duplicated - forming on both sides of the en expression stripes. In the lateral regions of these embryos, en expression is broken up into islands, each surrounded by an ectopic furrow.

The loss of segmentation and lack of smooth cuticle due to wgl-17/wgl-17 is partially maternally suppressed by AxnS044230/AxnS044230. If these embryos are also zygotically AxnS044230/AxnS044230, they produce cuticles consisting entirely of smooth cuticle, just as they would if they were wild-type for wg. arr::fz2arr.intra.Scer\UAS.T:Hsap\MYC; Scer\GAL4prd.RG1 restores smooth cuticle formation in wgl-17/wgl-17 embryos. No such effect is seen with fz2Scer\UAS.cCa; Scer\GAL4prd.RG1, fz2Scer\UAS.cTa.T:Hsap\MYC; Scer\GAL4prd.RG1 or fz2Scer\UAS.T:Avic\GFP-ECFP; Scer\GAL4prd.RG1.

The dorsal hole phenotype, loss of leading edge actin cable, and loss of adhesion between the amnioserosa and dorsal epidermis of hep1 mutant embryos are all partially suppressed by Scer\GAL469B with wgScer\UAS.cGa.

Has no effect on the eye phenotype produced by activated arm constructs. (either armS44Y.GMR or armS56F.GMR).

The addition of wgl-17 to dallygem/dally06464 flies, leads to enhancement of the posterior supraalar bristle phenotype seen in dallygem/dally06464 flies alone: 30% of flies have the phenotype, rather than 1%.

Many of the phenotypes caused by wgl-16/wgl-17 can be rescued by expression of Wnt4Scer\UAS.cGa under the control of Scer\GAL4ptc-559.1; wing rescue is seen at high frequency, halteres appear well developed, leg morphology is often rescued, but partial rescue of the antenna is only occasionally seen. The wing disc defect caused by shifting wgl-12/wgl-17 wing discs to the restrictive temperature for 24 hours at the beginning of the second larval instar can be rescued by expression of Wnt4Scer\UAS.cGa under the control of Scer\GAL4ptc-559.1 during the 24 hour period. When wgl-12/wgl-17 wing discs expressing Wnt4Scer\UAS.cGa under the control of Scer\GAL4ptc-559.1 are continuously maintained at the restrictive temperature from the second until the late third instar stage, the resulting discs fail to develop normally and remain very small.

In wgl-17 Wnt2unspecified double mutants in 40-45% of hemisegments, the dorsal trunk is completely missing, and in the remaining hemisegments only some reduced and thin dorsal trunk forms. Expression of armS10.Scer\UAS.T:Hsap\MYC under the control of Scer\GAL4btl.PS can substantially rescue the dorsal trunk which is missing in wgl-17 Wnt2unspecified double mutant embryos. Expression of Wnt2Scer\UAS.cSa under the control of Scer\GAL4wg.PM in a wgl-17 Wnt2unspecified double mutant background rescues some dorsal trunk in the trachea. However when Wnt2Scer\UAS.cSa is expressed under the control of Scer\GAL4btl.PS there is strong rescue, and more dorsal trunk is made. Expression of wgScer\UAS.cLa under the control of Scer\GAL4wg.PM in a wgl-17 Wnt2unspecified double mutant background rescues some dorsal trunk in the trachea. However when wgScer\UAS.cLa is expressed under the control of Scer\GAL4btl.PS there is strong rescue, and more dorsal trunk is made.

ci94 wgl-17 double mutant embryos are short and show a "lawn of denticles" phenotype.

Expression of slp1hs.PC in wgl-17 embryos rescues the RP2/sib lineage in as many as 85% of hemisegments. Rescue of NB4-2 is seen in approximately 43% of hemisegments. Expression of slp2hs.PC in wgl-8 or wgl-17 embryos rescues the RP2 lineage in approximately 50% of hemisegments.

Expression of Wnt4Scer\UAS.cGa under the control of Scer\GAL4da.G32 does not rescue the phenotype of wgl-17 embryos.

The wgl-17 phenotype is not affected by the expression of fz2Scer\UAS.cZa under the control of Scer\GAL4e22c.

Expression of Nrt::wgScer\UAS.T:Ivir\HA1 driven by Scer\GAL4wg.PM to wgl-17 flies rescues the phenotypes caused by wgl-17 alone.

enE wgl-17 double mutant embryos have segmentally repeated denticle whorls.

Dominantly enhances the wing notching phenotype caused by expression of argos::shgi.Scer\UAS.T:Hsap\MYC under the control of Scer\GAL4en-e16E. Dominantly suppresses the wing phenotype caused by expression of armScer\UAS.cWa under the control of Scer\GAL4en-e16E. Also, wing margin bristles are lost between veins 4 and 5.

The addition of wgl-17 also enhances the wing phenotype seen in mamN.Scer\UAS, Scer\GAL4C96 flies, in a partially penetrant manner, exhibiting loss of additional wing blade material along the posterior margin and bristle loss along the anterior margin. A small percentage of more sever strap wings is also observed.

The wgl-17 lawn of denticles phenotype is partially rescued if the embryos are also maternally and zygotically homozygous for Apc2ΔS; the normal diversity of cuticular pattern elements and small expanses of naked cuticle are restored.

Overexpression of fz2Scer\UAS.cCa under the control of Scer\GAL4e22c in a wgl-17/+ background results in cuticle patterning defects in 60% of embryos; ectopic denticles appear in the domain of cells that normally secrete naked cuticle.

wgl-17, ovosvb-2 double mutant embryos produce naked cuticle, with some residual abortive denticles. This phenotype is characteristic of ovosvb-2 embryos.

Expression of Nrt::wgScer\UAS.T:Ivir\HA1 driven by Scer\GAL4en-e16E in a wgl-17 background rescues an expanse of naked cuticle only 1-2 cells wide. Cuticle posterior to row 6 that would be naked in wild type are covered in additional denticles.

The wingless phenotype of wg1/wgl-17 flies is partially rescued by fz3G10; the fraction of flies with two wings increases from 46% to 87%, while the fraction of one wing and wingless flies reduces from 44% and 10% to 13% and 0.5% respectively.

Heat shock expression of dallyhs.PJ cannot rescue wgl-17. wgl-17 dominantly suppresses the genitalia defects seen in about 70% of dally06464/dallygem flies, so that abnormalities are only seen in less than 10% of flies.

Reducing the dose of maternally supplied gro gene product, using Df(3R)Espl22, suppresses the wg null phenotype. Paternal contribution of Df(3R)Espl22 has no effect.

Scer\GAL4dpp.blk1-mediated expression of vgScer\UAS.cKa restores the wing.

Clones of cells in the wing that are simultaneously mutant for wgl-17 and nub1 do not form ectopic bristle precursors.

The supernumerary wing bristle phenotypes of fz2Scer\UAS.cZa, Scer\GAL469B can be dominantly suppressed by wgl-17, though the polarity phenotype of fzScer\UAS.cZa, Scer\GAL469B cannot. The wing margin loss phenotype of fz2Scer\UAS.N, Scer\GAL469B can be slightly dominantly enhanced by wgl-17.

dpps4 wgl-17 embryos lack the second and third midgut constrictions.

Does not alter the eye tissue polarity phenotype produced by fzScer\UAS.cAa expressed under the control of Scer\GAL4hs.2sev.

The denticle phenotype of wgl-17 homozygous larvae is not altered if the larvae are also homozygous for Egfrf1 or are carrying EgfrDN.Scer\UAS (expressed under the control of Scer\GAL4arm.PS). Homozygous wgl-17 larvae derived from embryos in which spis.Scer\UAS is expressed under the control of Scer\GAL4arm.PS have lawns of denticles; these denticles are clearly smaller than those present in homozygous wgl-17 larvae that do not carry spis.Scer\UAS, and probably correspond to row 1-4 denticles.

Df(2R)enE wgl-17 embryos are small, spherical, carry a lawn of unpolarised denticles (A cell type denticles), have no Keilin's organs (presumably due to lack of functional parasegment boundaries) and the thoracic and abdominal identities are differentiated. Scer\GAL4arm.PS mediated expression of wgScer\UAS.cLa in wgl-17 Df(2R)enE embryos does not rescue segmentation, the embryos lengthen only a little and no Keilin's organs form. Instead of a lawn of denticles the ventral abdomen now makes naked cuticle. The T1 becomes largely covered by fine denticles normally found in the beard, the beard is not small and localised. Scer\GAL4arm.PS mediated expression of both wgScer\UAS.cLa and enScer\UAS.cGa in wgl-17 Df(2R)enE embryos causes a small beardless, near-spherical and unsegmented embryo with extruded organs (believed to be foregut and hindgut), i.e. less phenotypic rescue than for Scer\GAL4arm.PS mediated expression of wgScer\UAS.cLa alone. Scer\GAL4arm.PS mediated expression of both wgScer\UAS.cLa and hhScer\UAS.cIa in wgl-17 Df(2R)enE embryos causes naked cuticle to form in the place of the T1 beard. Scer\GAL4arm.PS mediated expression of wgl-12.Scer\UAS in wgl-17 Df(2R)enE embryos at varying temperatures can be used to study the dose response to wg for A cells. At 17.5oC wgl-12.Scer\UAS produces the same phenotype as when wild type wg (wgScer\UAS.cLa) is added. At 20oC there are only a few ventral denticles and some beard in T1. At 22oC there are two lateral stripes of ventral denticles and some beard in T1. At 23oC the abdomen is completely covered in denticles but there is no beard in T1. At 25oC the abdomen is completely covered in denticles, weak thoracic denticles are present, but there is no beard in T1. At 28.5oC embryos are indistinguishable from wgl-17 Df(2R)enE embryo. Scer\GAL4prd.RG1 mediated expression of wgScer\UAS.cLa in wgl-17 Df(2R)enE embryos causes a lengthening of the whole embryo and instead of a lawn of denticles alternate stripes of naked and denticulate cuticle appear. Two types of denticle form in each band, small ones on the outside and larger ones inward. Individual denticles tend to point towards the nearest naked domain.

Heart formation does not occur in dshhs.PA, wgl-17 flies reared at 25oC or 27oC. Heat shock for 30 minutes between 3 and 4 hours of development rescues heart development, often flies exhibit cardiac hyperplasia.

wgl-17 Pka-C1E95 clones cause local outgrowths of leg tissue and on rare occasions form of supernumerary legs.

Partially suppression of the defects caused by Pka-C1H2 clones in the ventral regions of the leg, without affecting the majority of pattern defects in the wing, notum, halteres and antennae.

ptc9, wgl-17 double mutants have lateral whirls of denticles.

Xenogenetic Interactions
Statement
Reference

Expression of BacA\p35Scer\UAS.cHa driven by Scer\GAL4hh-Gal4 in posterior wing compartments composed of homozygous wgl-17 mutant cells does not substantially restore normal wing size.

The neoplastic tumours induced by wgl-17 mutant cells blocked for apoptosis (described in FBrf0191458) appear to be due to the loss of l(2)gl function from the mutant chromosome studied.

FlyBase curator comment: The neoplastic tumours induced by wgl-17 mutant cells blocked for apoptosis (described in FBrf0191458) appear to be due to the loss of l(2)gl function from the mutant chromosome studied and not due to an affect of the wgl-17 mutation (see FBrf0207678).

X-ray irradiated wing disc clones expressing BacA\p35Scer\UAS.cHa under the control of Scer\GAL4tub in wgl-17 contain a mixture of two types of cell: `live' cells, which have not initiated apoptosis due to the irradiation, and `undead' cells (between 20 and 70% of the clone), which have initiated apoptosis, but have failed to complete programmed cell death. No such cells persist outside the clones in which BacA\p35Scer\UAS.cHa is expressed. X-ray irradiated wing disc clones expressing BacA\p35Scer\UAS.cHa under the control of Scer\GAL4tub in dppd12 wgl-17 mutants contain a mixture of two types of cell: `live' cells, which have not initiated apoptosis due to the irradiation, and `undead' cells (between 20 and 70% of the clone), which have initiated apoptosis, but have failed to complete programmed cell death. No such cells persist outside the clones in which BacA\p35Scer\UAS.cHa is expressed. Unlike BacA\p35Scer\UAS.cHa (Scer\GAL4tub) wing disc clones, BacA\p35Scer\UAS.cHa (Scer\GAL4tub) dppd12 wgl-17 clones appear to be associated with extra proliferation or growth after stress (such as X-ray irradiation). Clones expressing BacA\p35Scer\UAS.cHa under the control of Scer\GAL4tub in wgl-17 X-ray irradiated wing discs fall into two classes. Clones in the first class do not contain `undead' cells and grow normally. Clones in the second class contain clusters of `undead' cells and overgrow dramatically, forming disorganised masses of tissue that lose the original monolayer organisation characteristic of the wing disc epithelium and instead behave like neoplastic tumors that often bulge out from the main body of the disc. These overproliferating clones tend to fuse, forming large single patches that cover the greater part of the disc, and in many cases (approximately 27%) they seem to constitute the entire disc. BacA\p35Scer\UAS.cHa (Scer\GAL4tub) wgl-17 clones that include `undead' cells proliferate at a much higher rate than the surrounding tissue. However, `undead' cells within these clones divide only rarely, indicating that it is the remaining, live cells within the clones that overgrow. In contrast, no such overgrowth or overproliferation is observed in corresponding control discs containing unstressed clones, or BacA\p35Scer\UAS.cHa (Scer\GAL4tub) dppd12 wgl-17 clones. Co-expression of rprScer\UAS.cZa with BacA\p35Scer\UAS.cHa (both under the control of Scer\GAL4unspecified) in wgl-17 wing disc clones results in most or all of the cells in the clone being `undead'. None of these clones are associated with large, neoplastic outgrowths, and they grow slowly, forming abnormally small clones.

Complementation and Rescue Data
Partially rescued by
Comments

Expression of wgScer\UAS.cHa under the control of Scer\GAL4prd.RG1 in wgl-17 embryos fully rescues naked cuticle in odd-numbered segments and substantially rescues denticle diversity in the epidermal cells adjacent to the Scer\GAL4prd.RG1 expression domain.

Expression of wgS239A.Scer\UAS.T:Ivir\HA1 driven by Scer\GAL4hh-Gal4 in posterior wing compartments composed of homozygous wgl-17 mutant cells substantially restores wing size and the rate of cell proliferation. Rescued wings appear well proportioned, but they lack a proper margin in the posterior compartment.

Expression of wgScer\UAS.cGa under the control of Scer\GAL4pros.PMG partially rescues the loss of naked cuticle in wgl-17 larvae, but reduces denticle diversity. This expression restores RP2 neurons to wgl-17 embryos.

wgScer\UAS.cGa; Scer\GAL4da.G32 rescues the loss of naked ventral cuticle in wgl-17 homozygous embryos. About half of the resulting embryos have the wgScer\UAS.cGa; Scer\GAL4da.G32 overexpression phenotype of a completely naked ventral cuticle. wgScer\UAS.cGa; Scer\GAL4da.G32 rescues the dorsal-ventral elongation and orientation of microtubule bundles in the leading edge cells of stage 13 wgl-17 homozygous embryos. wgScer\UAS.cGa; Scer\GAL4332.3 rescues the dorsal-ventral polarity of leading edge cells in these embryos, including orientation of the microtubule bundles. But dorsal-ventral elongation of these cells is not rescued. tkvQ253D.Scer\UAS.cNb; Scer\GAL4da.G32 only weakly rescues polarisation of leading edge cells in stage 13 wgl-17 homozygous embryos, and fails to rescue elongation of these cells.

wgScer\UAS.cGa; Scer\GAL4da.G32 s the polarity and organization of leading edge cells during dorsal closure in wgl-17 mutant embryos.

When wgScer\UAS.T:λ\cI-hinge,T:Arus\HRP is driven by Scer\GAL4wg.PM in wgl-17 mutants, the phenotypes are extensively rescued, the cuticular pattern, including the polarity and shape of individual denticles is completely restored in many segments. In some segments rescue is incomplete, as some denticle belts remain fused.

wgPE2.Scer\UAS rescues denticle diversity in wgl-17 larvae when driven by Scer\GAL4e22c.

Expression of wgScer\UAS.cLa driven by Scer\GAL4en-e16E in a wgl-17 background rescues many rows of the denticle belts, except row 1.

wgPE6.Scer\UAS fails to rescue the dorsal cuticle pattern of wgl-17 embryos when expressed under the control of Scer\GAL4e22c at 25oC. wgPE6.Scer\UAS substantially rescues dorsal pattern elements in wgl-17 embryos when expressed under the control of Scer\GAL4e22c at 18oC. wgNE1.Scer\UAS fails to rescue the dorsal cuticle pattern of wgl-17 embryos when expressed under the control of Scer\GAL4e22c at 18oC.

wgl-17 embryos expressing wgScer\UAS.cHa or wgScer\UAS.cHa.T:Ivir\HA1 under the control of Scer\GAL4wg.PM show full rescue of the ventral cuticle pattern, although the embryos are slightly distorted as the dorsal pattern elements are not rescued. Expression of wgPE2.Scer\UAS or wgPE2.Scer\UAS.T:Ivir\HA1 using Scer\GAL4wg.PM in wgl-17 embryos rescues denticle diversity, but there is no specification of naked cuticle. Expression of wgPE4.Scer\UAS or wgPE4.Scer\UAS.T:Ivir\HA1 using Scer\GAL4wg.PM in wgl-17 embryos rescues naked cuticle, but these embryos show little denticle diversity.

Images (0)
Mutant
Wild-type
Stocks (3)
Notes on Origin
Discoverer

Baker.

Comments
Comments

The expression of l(1)sc is unaltered in early homozygous mutant embryos.

Derepression of en in Pc group mutants is not acting through wg.

gsb-n protein expression has been studied in wgl-17 embryos.

The wg phenotype is suppressed by mutations in nkd and enhanced by mutations in hh.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (13)
Reported As
Symbol Synonym
wg (CX4)
wgCX4
(Lybrand et al., 2019, Won et al., 2019, Huang et al., 2018, Ogura et al., 2018, Ripp et al., 2018, Recasens-Alvarez et al., 2017, Rizzo and Bejsovec, 2017, Yamazaki et al., 2016, Yang et al., 2016, Alexandre et al., 2014, Herrero et al., 2014, Linnemannstöns et al., 2014, Wang and Page-McCaw, 2014, Paul et al., 2013, Bejsovec and Chao, 2012, Yang et al., 2012, Cordero and Cagan, 2010, Jones et al., 2010, Monier et al., 2010, Sotillos et al., 2010, Baena-Lopez et al., 2009, Chang et al., 2008, Chao et al., 2007, Zecca and Struhl, 2007, Estrada et al., 2006, Mirkovic and Mlodzik, 2006, Singh et al., 2006, Chen et al., 2005, Cox and Baylies, 2005, Cox et al., 2005, Franch-Marro et al., 2005, Jones and Bejsovec, 2005, Lim et al., 2005, Merabet et al., 2005, Perez-Garijo et al., 2005, Buescher et al., 2004, Bullock et al., 2004, Cordero et al., 2004, De Velasco et al., 2004, Mandal et al., 2004, Morel and Arias, 2004, Wang and Struhl, 2004, Alexandre and Vincent, 2003, Desbordes and Sanson, 2003, Grienenberger et al., 2003, Hosono et al., 2003, Landgraf et al., 2003, Larsen et al., 2003, Reim et al., 2003, Tolwinski et al., 2003, Angelats et al., 2002, Bauer et al., 2002, Cadigan et al., 2002, Cavodeassi et al., 2002, Glise et al., 2002, Kaltschmidt et al., 2002, Parker et al., 2002, Pfeiffer et al., 2002, Streit et al., 2002, Sudarsan et al., 2002, Tang and Sun, 2002, Buratovich and Wilder, 2001, Deshpande et al., 2001, Dubois et al., 2001, Fuss et al., 2001, Gieseler et al., 2001, Keisman and Baker, 2001, Knirr and Frasch, 2001, Llimargas and Lawrence, 2001, Marty et al., 2001, Methot and Basler, 2001, San Martin and Bate, 2001, Simmonds et al., 2001, Thumm and Kadowaki, 2001, Bhat et al., 2000, Fanto, 2000, Fanto et al., 2000, Halfon et al., 2000, Llimargas, 2000, Moline et al., 2000, Pfeiffer et al., 2000, Rusch and Kaufman, 2000, Wan et al., 2000, Wang et al., 2000, Zeng et al., 2000, Adachi-Yamada et al., 1999, Bhanot et al., 1999, Brennan et al., 1999, Chen and Struhl, 1999, de Celis et al., 1999, Gallet et al., 1999, Garcia-Garcia et al., 1999, Gieseler et al., 1999, Gorfinkiel et al., 1999, Greaves et al., 1999, Hays et al., 1999, Helms et al., 1999, Lin et al., 1999, McCartney et al., 1999, Micchelli and Blair, 1999, Moline et al., 1999, Rollins et al., 1999, Sanson et al., 1999, Sato et al., 1999, Tsuda et al., 1999, Bachmann and Knust, 1998, Bhat, 1998, Bilder and Scott, 1998, Cadigan et al., 1998, Carmena et al., 1998, Cavallo et al., 1998, Dierick and Bejsovec, 1998, Fuss and Hoch, 1998, Gajewski et al., 1998, Gallet et al., 1998, Gallitano-Mendel and Finkelstein, 1998, Klein and Martinez Arias, 1998, Martinez Arias, 1998, Nakagoshi et al., 1998, Neumann and Cohen, 1998, Richter et al., 1998, Wehrli and Tomlinson, 1998, White et al., 1998, Zhang and Carthew, 1998, Bhat and Schedl, 1997, Buratovich et al., 1997, Chen and Baker, 1997, Dominguez and Hafen, 1997, Duman-Scheel et al., 1997, Emerald and Roy, 1997, Gallitano-Mendel and Finkelstein, 1997, Hays et al., 1997, Jagla et al., 1997, McDonald and Doe, 1997, Micchelli et al., 1997, Neumann and Cohen, 1997, Shishido et al., 1997, Struhl et al., 1997, Strutt et al., 1997, Treisman et al., 1997, Zhou et al., 1997, Bhat, 1996, Buttgereit, 1996, Cadigan and Nusse, 1996, Held and Heup, 1996, Jiang and Struhl, 1996, Lawrence et al., 1996, Ma et al., 1996, Mann and Abu-Shaar, 1996, Morcillo et al., 1996, Neumann and Cohen, 1996, Neumann and Cohen, 1996, Park et al., 1996, Ranganayakulu et al., 1996, Uemura et al., 1996, van den Heuvel and Ingham, 1996, Wilk et al., 1996, Zecca et al., 1996, Baylies et al., 1995, Bejsovec and Wieschaus, 1995, Cimbora and Sakonju, 1995, Jiang and Struhl, 1995, Lawrence et al., 1995, Li et al., 1995, Pan and Rubin, 1995, Hartenstein et al., 1994, Heemskerk and DiNardo, 1994, Jackson and Hoffmann, 1994, Kaphingst and Kunes, 1994, Klingensmith et al., 1994, Lawrence et al., 1994, Noordermeer et al., 1994, Theisen et al., 1994, Vincent and Lawrence, 1994, Bejsovec and Wieschaus, 1993, Phillips and Whittle, 1993, Sampedro et al., 1993, van den Heuvel et al., 1993, van den Heuvel et al., 1993, Gonzalez-Reyes et al., 1992, Moazed and O'Farrell, 1992, Ouellette et al., 1992, Gonzalez et al., 1991, Heemskerk et al., 1991, Martin-Bermudo et al., 1991, Parkhurst and Ish-Horowicz, 1991, Kassis, 1990, Simcox et al., 1989, Tremml and Bienz, 1989, Baker, 1987)
Name Synonyms
Secondary FlyBase IDs
    References (272)