Polytene chromosomes normal.
alar lobe (with wgspd-fg:Sp-1)
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
eye disc | heat sensitive (with wgl-12)
larval hindgut & ectoderm
retina | pupal stage | heat sensitive (with wgl-12)
wing (with wgspd-fg:Sp-1)
wing disc | heat sensitive (with wgl-12)
wing margin (with wgspd-fg:Sp-1)
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 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.
The RNA-null wgl-17 mutant produces a 'lawn of denticles' phenotype.
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.
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 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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
Mutant embryos have a lawn of row-5-type ventral denticles, with segmental polarity reversals.
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.
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
wgl-17 has decreased cell number | embryonic stage phenotype, non-enhanceable by ptc9
wgSp-1/wgl-17 has visible phenotype, suppressible by pnrSA.UAS.β/Scer\GAL4pnr-MD237
wgSp-1/wgl-17 has visible phenotype, suppressible by Scer\GAL4pnr-MD237/scSA.UAS
wg1/wgl-17 has visible phenotype, suppressible by HipkUAS.Tag:HA/Scer\GAL469B
wgl-16/wgl-17 has visible phenotype, suppressible | partially by Scer\GAL4ptc-559.1/Wnt4UAS.cGa
wg[+]/wgl-17 is an enhancer of visible | adult stage phenotype of Scer\GAL4sd.PU, domeKK104700
wgl-17 is an enhancer of visible phenotype of Nsf2EQ.UAS, Scer\GAL4bbg-C96
wgl-17 is an enhancer of visible phenotype of Scer\GAL4unspecified, nkdUAS.cZa
wg[+]/wgl-17 is an enhancer of visible phenotype of Scer\GAL4en-e16E, shgi.UAS.Tag:SS(aos),Tag:MYC
wgl-17 is an enhancer of visible phenotype of Scer\GAL4GMR.PF, shgi.UAS.Tag:SS(aos),Tag:MYC
wgl-17 is an enhancer of visible phenotype of Scer\GAL4bbg-C96, mamN.UAS
wgl-17 is an enhancer of visible phenotype of Scer\GAL469B, fz2UAS.N
wg[+]/wgl-17 is a suppressor of abnormal size phenotype of Scer\GAL4GMR.PF, egrUAS.cIa
wg[+]/wgl-17 is a suppressor of visible phenotype of Scer\GAL4GMR.PF, egrUAS.cIa
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 visible phenotype of NGD144, Scer\GAL4sev.PU
wg[+]/wgl-17 is a suppressor | partially of decreased cell number | third instar larval stage phenotype of NGD144, Scer\GAL4sev.PU
wg[+]/wgl-17 is a suppressor of abnormal size | adult stage phenotype of Nspl-1
wg[+]/wgl-17 is a suppressor of decreased cell number | third instar larval stage phenotype of Nspl-1
wgl-17 is a suppressor of abnormal neuroanatomy | embryonic stage phenotype of midlos1
wgl-17 is a suppressor of decreased cell number | embryonic stage phenotype of ptc9
wgl-17 is a suppressor of visible phenotype of Scer\GAL4GMR.PF, armUAS.cWa
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
wgl-17 is a non-suppressor of abnormal planar polarity phenotype of Scer\GAL469B, fzUAS.cZa
wgl-17 is a non-suppressor of abnormal planar polarity phenotype of Scer\GAL4hs.2sev, fzUAS.cAa
wgl-17 has embryonic/first instar larval cuticle phenotype, enhanceable by dshΔDIX.UAS/Scer\GAL4da.G32
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 embryonic/first instar larval cuticle phenotype, suppressible by pan2
wgSp-1/wgl-17 has dorsocentral bristle phenotype, suppressible by pnrSA.UAS.β/Scer\GAL4pnr-MD237
wgSp-1/wgl-17 has dorsocentral bristle phenotype, suppressible by Scer\GAL4pnr-MD237/scSA.UAS
wg1/wgl-17 has wing phenotype, suppressible by HipkUAS.Tag:HA/Scer\GAL469B
wg1/wgl-17 has mesonotum | ectopic phenotype, suppressible by HipkUAS.Tag:HA/Scer\GAL469B
wgl-17 has embryonic/first instar larval cuticle phenotype, suppressible by SoxNNC14
wgl-17 has ventral denticle belt phenotype, suppressible by SoxNNC14
wgl-17 has abdominal lateral oblique muscle 1 founder cell phenotype, suppressible by Scer\GAL4twi.PB/twiUAS.cBa
wgl-17 has abdominal ventral transverse muscle 1 founder cell phenotype, suppressible by Scer\GAL4twi.PB/twiUAS.cBa
wgl-17 has abdominal ventral acute muscle 1 founder cell phenotype, suppressible by Nrt::wgScer\FRT-.UAS.Tag:HA/Scer\GAL4wg.PM
wgl-17 has abdominal ventral acute muscle 2 founder cell phenotype, suppressible by Nrt::wgScer\FRT-.UAS.Tag:HA/Scer\GAL4wg.PM
wgl-17 has abdominal ventral acute muscle 3 founder cell phenotype, suppressible by Nrt::wgScer\FRT-.UAS.Tag:HA/Scer\GAL4wg.PM
wgl-17 has abdominal lateral oblique muscle 1 founder cell phenotype, suppressible by Nrt::wgScer\FRT-.UAS.Tag:HA/Scer\GAL4wg.PM
wgl-17 has denticle | ectopic phenotype, suppressible by Scer\GAL4da.G32/dshΔDEP+.UAS
wgl-17 has denticle | ectopic phenotype, suppressible by dshUAS.cAa/Scer\GAL4da.G32
wgl-17 has embryonic leading edge cell primordium & microtubule phenotype, suppressible by armS10.UAS.Tag:MYC/Scer\GAL4da.G32
wgl-17 has embryonic leading edge cell primordium phenotype, suppressible by armS10.UAS.Tag:MYC/Scer\GAL4da.G32
wgl-17 has embryonic leading edge cell primordium phenotype, suppressible by Scer\GAL4da.G32/dshΔDEP+.UAS
wgl-17 has embryonic leading edge cell primordium phenotype, suppressible by dshUAS.cAa/Scer\GAL4da.G32
wgl-17 has embryonic/first instar larval cuticle phenotype, suppressible by Scer\GAL4da.G32/dshΔDEP+.UAS
wgl-17 has embryonic/first instar larval cuticle phenotype, suppressible by dshUAS.cAa/Scer\GAL4da.G32
wgl-17 has denticle | ectopic phenotype, suppressible by armS10.UAS.Tag:MYC/Scer\GAL4da.G32
wgl-17 has ventral denticle belt | ectopic phenotype, suppressible by Scer\GAL4prd.RG1/arr::fz2arr.intra.UAS.Tag:MYC
wgl-17 has embryonic/first instar larval cuticle phenotype, suppressible by Scer\GAL4prd.RG1/arr::fz2arr.intra.UAS.Tag:MYC
wgl-17 has embryonic/first instar larval cuticle phenotype, suppressible by AxnS044230
wgl-17 has ventral denticle belt | ectopic phenotype, suppressible by AxnS044230
wgl-16/wgl-17 has antenna phenotype, suppressible | partially by Scer\GAL4ptc-559.1/Wnt4UAS.cGa
wgl-16/wgl-17 has wing disc phenotype, suppressible by Scer\GAL4ptc-559.1/Wnt4UAS.cGa
wgl-16/wgl-17 has haltere phenotype, suppressible by Scer\GAL4ptc-559.1/Wnt4UAS.cGa
wgl-16/wgl-17 has leg phenotype, suppressible by Scer\GAL4ptc-559.1/Wnt4UAS.cGa
wgl-16/wgl-17 has mesonotum | ectopic phenotype, suppressible by Scer\GAL4ptc-559.1/Wnt4UAS.cGa
wgl-16/wgl-17 has wing phenotype, suppressible by Scer\GAL4ptc-559.1/Wnt4UAS.cGa
wgl-12/wgl-17 has wing disc phenotype, suppressible | partially by Scer\GAL4ptc-559.1/Wnt4UAS.cGa
Wnt2unspecified, wgl-17 has tracheal dorsal trunk primordium phenotype, suppressible by armS10.UAS.Tag:MYC/Scer\GAL4btl.PS
Wnt2unspecified, wgl-17 has tracheal dorsal trunk primordium phenotype, suppressible | partially by Wnt6UAS.cSa/Scer\GAL4btl.PS
Wnt2unspecified, wgl-17 has tracheal dorsal trunk primordium phenotype, suppressible | partially by Wnt6UAS.cSa/Scer\GAL4wg.PM
Wnt2unspecified, wgl-17 has tracheal dorsal trunk primordium phenotype, suppressible | partially by wntDUAS.cSa/Scer\GAL4btl.PS
Wnt2unspecified, wgl-17 has tracheal dorsal trunk primordium phenotype, suppressible | partially by wntDUAS.cSa/Scer\GAL4wg.PM
wgl-17 has hindgut visceral muscle primordium phenotype, suppressible by armS10.UAS.Tag:MYC/Scer\GAL4455.2
wgl-17 has hindgut visceral muscle primordium phenotype, suppressible by Scer\GAL4twi.PB/armS10.UAS.Tag:MYC
wgl-17 has RP2sib neuron phenotype, suppressible by slp1hs.PC
wgl-17 has neuroblast NB4-2 phenotype, suppressible by slp1hs.PC
wgl-17 has larval RP2 motor neuron phenotype, suppressible by slp1hs.PC
wgl-17 has larval RP2 motor neuron phenotype, suppressible by slp2hs.PC
wgl-17/Df(2L)DE has phenotype, suppressible | partially by dallyhs.PJ
wgl-17 has phenotype, suppressible by Nrt::wgUAS.Tag:HA/Scer\GAL4wg.PM
wgl-17 has embryonic/first instar larval cuticle phenotype, suppressible by Apc2ΔS
wgl-17 has embryonic epidermis phenotype, suppressible by ovosvb-2
wgl-17 has ventral denticle belt phenotype, suppressible by ovosvb-2
wgl-17 has embryonic epidermis phenotype, suppressible by Df(3R)Espl22
wgl-17 has ventral denticle belt phenotype, suppressible by Df(3R)Espl22
wgl-17 has embryonic epidermis phenotype, suppressible by pan3
wgl-17 has ventral denticle belt phenotype, suppressible by pan3
wgl-16/wgl-17 has wing phenotype, suppressible by Scer\GAL4dpp.blk1/vgUAS.cKa
wgl-17 has embryonic/larval dorsal vessel phenotype, suppressible by dshhs.PA
wgl-17 has abdominal ventral acute muscle 1 founder cell phenotype, non-suppressible by Scer\GAL4twi.PB/twiUAS.cBa
wgl-17 has abdominal ventral acute muscle 2 founder cell phenotype, non-suppressible by Scer\GAL4twi.PB/twiUAS.cBa
wgl-17 has abdominal ventral acute muscle 3 founder cell phenotype, non-suppressible by Scer\GAL4twi.PB/twiUAS.cBa
wgl-17 has denticle | ectopic phenotype, non-suppressible by dshΔDIX.UAS/Scer\GAL4da.G32
wgl-17 has embryonic leading edge cell primordium & microtubule phenotype, non-suppressible by armS10.UAS.Tag:MYC/Scer\GAL4332.3
wgl-17 has embryonic leading edge cell primordium phenotype, non-suppressible by armS10.UAS.Tag:MYC/Scer\GAL4332.3
wgl-17 has ventral denticle belt | ectopic phenotype, non-suppressible by Scer\GAL4prd.RG1/fz2UAS.ECFP
wgl-17 has ventral denticle belt | ectopic phenotype, non-suppressible by Scer\GAL4prd.RG1/fz2UAS.cTa.Tag:MYC
wgl-17 has ventral denticle belt | ectopic phenotype, non-suppressible by Scer\GAL4prd.RG1/fz2UAS.cCa
wgl-17 has embryonic/first instar larval cuticle phenotype, non-suppressible by Scer\GAL4prd.RG1/fz2UAS.ECFP
wgl-17 has embryonic/first instar larval cuticle phenotype, non-suppressible by Scer\GAL4prd.RG1/fz2UAS.cTa.Tag:MYC
wgl-17 has embryonic/first instar larval cuticle phenotype, non-suppressible by Scer\GAL4prd.RG1/fz2UAS.cCa
Wnt2unspecified, wgl-17 has tracheal dorsal trunk primordium phenotype, non-suppressible by Wnt10UAS.cSa/Scer\GAL4btl.PS
Wnt2unspecified, wgl-17 has tracheal dorsal trunk primordium phenotype, non-suppressible by Wnt10UAS.cSa/Scer\GAL4wg.PM
Wnt2unspecified, wgl-17 has tracheal dorsal trunk primordium phenotype, non-suppressible by Wnt4UAS.cSa/Scer\GAL4btl.PS
Wnt2unspecified, wgl-17 has tracheal dorsal trunk primordium phenotype, non-suppressible by Wnt4UAS.cSa/Scer\GAL4wg.PM
Wnt2unspecified, wgl-17 has tracheal dorsal trunk primordium phenotype, non-suppressible by Wnt5UAS.cSa/Scer\GAL4btl.PS
Wnt2unspecified, wgl-17 has tracheal dorsal trunk primordium phenotype, non-suppressible by Wnt5UAS.cSa/Scer\GAL4wg.PM
wgl-17 has hindgut visceral muscle primordium phenotype, non-suppressible by Scer\GAL4how-24B/armS10.UAS.Tag:MYC
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
wg[+]/wgl-17 is an enhancer of wing hair | ectopic phenotype of armNdel.vg.MQ
wg[+]/wgl-17 is an enhancer of wing margin bristle | decreased number phenotype of Arf61
wg[+]/wgl-17 is an enhancer of wing margin bristle | decreased number phenotype of Arf6GX16w-
wg[+]/wgl-17 is an enhancer of mesonotum | adult stage | ectopic phenotype of Scer\GAL4sd.PU, domeKK104700
wg[+]/wgl-17 is an enhancer of ventral denticle belt phenotype of Cow5Δ
wg[+]/wgl-17 is an enhancer of abdominal ventral denticle belt | embryonic stage phenotype of Scer\GAL4e22c, pavUASp.mGFP6, tumUAS.cSa
wgl-17 is an enhancer of denticle phenotype of Scer\GAL469B, ciUAS.cAa
wgl-17 is an enhancer of embryonic/first instar larval cuticle phenotype of Scer\GAL469B, ciUAS.cAa
wgl-17/Scer\GAL469B is an enhancer of embryonic epidermis phenotype of ciUAS.cAa
wgl-17 is an enhancer of posterior supraalar bristle phenotype of dallygem/dally06464
wgl-17 is an enhancer of wing margin phenotype of Nsf2EQ.UAS, Scer\GAL4bbg-C96
wg[+]/wgl-17 is an enhancer of wing phenotype of Scer\GAL4en-e16E, shgi.UAS.Tag:SS(aos),Tag:MYC
wgl-17 is an enhancer of eye phenotype of Scer\GAL4GMR.PF, shgi.UAS.Tag:SS(aos),Tag:MYC
wg[+]/wgl-17 is an enhancer of wing margin phenotype of ctL32, su(Hw)e2
wgl-17 is a non-enhancer of genital disc phenotype of ix1
wgl-17 is a non-enhancer of embryonic/first instar larval cuticle phenotype of AxnS044230
wg[+]/wgl-17 is a suppressor of eye phenotype of Scer\GAL4GMR.PF, egrUAS.cIa
wg[+]/wgl-17 is a suppressor of stalk follicle cell | increased number | heat sensitive phenotype of Df(2R)BSC132/Mmp2Y53N
wg[+]/wgl-17 is a suppressor | partially of cone cell phenotype of NGD144, Scer\GAL4sev.PU
wg[+]/wgl-17 is a suppressor | partially of eye phenotype of NGD144, Scer\GAL4sev.PU
wg[+]/wgl-17 is a suppressor of photoreceptor phenotype of Nspl-1
wgl-17 is a suppressor of larval RP2 motor neuron | ectopic phenotype of midlos1
Scer\GAL4twi.PB/wgl-17 is a suppressor of abdominal ventral transverse muscle 1 founder cell phenotype of twiUAS.cBa
wg[+]/wgl-17 is a suppressor of ventral denticle belt phenotype of nkd2
wg[+]/wgl-17 is a suppressor of embryonic/first instar larval cuticle phenotype of nkd2
wgl-17 is a suppressor of arista | increased number phenotype of obk1
wgl-17 is a suppressor of eye phenotype of Scer\GAL4GMR.PF, armUAS.cWa
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 of wing margin bristle | ectopic | somatic clone phenotype of nub1
wgl-17 is a suppressor of wing sensillum | ectopic phenotype of Scer\GAL469B, fz2UAS.cZa
wgl-17 is a suppressor of leg | somatic clone phenotype of Pka-C1H2
wgl-17 is a non-suppressor of genital disc phenotype of ix1
wgl-17 is a non-suppressor of ventral 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
wgl-17 is a non-suppressor of wing margin bristle phenotype of Scer\GAL469B, fzUAS.cZa
Scer\GAL4prd.RG1, dshUAS.cAa, wgl-17 has embryonic/first instar larval cuticle | maternal effect phenotype
Scer\GAL4prd.RG1, dshUAS.cAa, wgl-17 has ventral denticle belt | maternal effect phenotype
ptc9, wgl-17 has genital disc primordium phenotype
Scer\GAL4twi.PB, twiUAS.cBa, wgl-17 has abdominal ventral acute muscle 1 founder cell phenotype
Scer\GAL4twi.PB, twiUAS.cBa, wgl-17 has abdominal ventral acute muscle 2 founder cell phenotype
Scer\GAL4twi.PB, twiUAS.cBa, wgl-17 has abdominal ventral acute muscle 3 founder cell phenotype
Scer\GAL4e22c, nkdUAS.cZa, wg[+]/wgl-17 has embryonic/first instar larval cuticle phenotype
Scer\GAL4e22c, nkdUAS.cZa, wgl-17 has embryonic/first instar larval cuticle phenotype
Scer\GAL4αTub84B.PP, ciUAS.cAa, wgl-17 has embryonic/first instar larval cuticle phenotype
Scer\GAL4wg.PM, ciUAS.cAa, wgl-17 has embryonic/first instar larval cuticle phenotype
Wnt2unspecified, wgl-17 has tracheal dorsal trunk primordium phenotype
ci94, wgl-17 has ventral denticle belt phenotype
ci94, wgl-17 has embryonic/first instar larval cuticle phenotype
Scer\GAL4en-e16E, armUAS.cWa, wgl-17 has wing margin bristle phenotype
Scer\GAL4en-e16E, armUAS.cWa, wg[+]/wgl-17 has wing margin bristle phenotype
Scer\GAL4en-e16E, armS10.UAS.Tag:MYC, wgl-17 has embryonic epidermis phenotype
Scer\GAL4en-e16E, armS10.UAS.Tag:MYC, wgl-17 has ventral denticle belt phenotype
Scer\GAL4e22c, fz2UAS.cCa, wg[+]/wgl-17 has ventral denticle belt phenotype
Scer\GAL4e22c, fz2UAS.cCa, wg[+]/wgl-17 has embryonic/first instar larval cuticle phenotype
Scer\GAL4e22c, fz2UAS.cCa, wgl-17 has ventral denticle belt phenotype
Scer\GAL4e22c, fz2UAS.cCa, wgl-17 has embryonic/first instar larval cuticle phenotype
Scer\GAL4e22c, panΔN.UAS, wgl-17 has embryonic epidermis phenotype
Scer\GAL4e22c, panΔN.UAS, wgl-17 has ventral denticle belt phenotype
dpps4, wgl-17 has embryonic midgut constriction 2 phenotype
dpps4, wgl-17 has embryonic midgut constriction 3 phenotype
Df(2R)enE, wgl-17 has embryonic/first instar larval cuticle phenotype
Df(2R)enE, wgl-17 has Keilin organ phenotype
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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).
wgl-17 is rescued by wgUAS.cGa/Scer\GAL4da.G32
wgl-17 is rescued by Scer\GAL4en-e16E/wgUAS.GFP
wgl-17 is rescued by wgUAS.GFP/Scer\GAL4wg.PM
wgl-17 is rescued by wgPE2.UAS/Scer\GAL4e22c
wgl-17 is rescued by wgΔ85.UAS/Scer\GAL4prd.RG1
wgl-17 is rescued by Scer\GAL4prd.RG1/wgΔ85.UAS.Tag:HA
wgl-17 is rescued by wgUAS.cHa.Tag:HA/Scer\GAL4wg.PM
wgl-17 is rescued by wghs.Tag:HA
wgl-17 is rescued by wgUAS.cHa/Scer\GAL4wg.PM
wgl-17 is rescued by wgPE4.hs.Tag:HA
wgGal4/wgl-17 is partially rescued by Scer\GAL4wg-Gal4/wgUAS.GFP
wgl-17 is partially rescued by Scer\GAL4prd.RG1/wgUAS.cHa
wgl-17 is partially rescued by Scer\GAL4hh-Gal4/wgS239A.UAS.Tag:HA
wgl-17 is partially rescued by Scer\GAL4pros.PMG/wgUAS.cGa
wgl-17 is partially rescued by wgUAS.cGa/Scer\GAL4332.3
wgl-17 is partially rescued by wgUAS.cGa/Scer\GAL4da.G32
wgl-17 is partially rescued by wgUAS.HRP/Scer\GAL4wg.PM
wgl-17 is partially rescued by wgwg.3'UTR.UAS/Scer\GAL4wg.PM
wgl-17 is partially rescued by wgSV40.3'UTR.UAS/Scer\GAL4wg.PM
wgl-17 is partially rescued by Scer\GAL4en-e16E/wgUAS.cLa
wgl-17 is partially rescued by wgPE6.UAS/Scer\GAL4e22c
wgl-17 is partially rescued by wgPE2.UAS.Tag:HA/Scer\GAL4wg.PM
wgl-17 is partially rescued by Scer\GAL4e22c/wgPE2.UAS.Tag:HA
wgl-17 is partially rescued by wgPE4.UAS/Scer\GAL4wg.PM
wgl-17 is partially rescued by wgPE2.hs.Tag:HA
wgl-17 is partially rescued by wgPE2.UAS/Scer\GAL4wg.PM
wgl-17 is partially rescued by wgPE2.UAS/Scer\GAL4e22c
wgl-17 is partially rescued by wgPE4.UAS.Tag:HA/Scer\GAL4wg.PM
wgGal4/wgl-17 is not rescued by wgCTD.UAS.Tag:MYC/Scer\GAL4wg-Gal4
wgl-17 is not rescued by wgPpa.3'UTR.UAS/Scer\GAL4wg.PM
wgl-17 is not rescued by wgPE6.UAS/Scer\GAL4e22c
wgl-17 is not rescued by Scer\GAL4e22c/wgNE1.UAS
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.
Baker.
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.