|Feature type||allele||Associated gene||Dmel\wg|
|Also Known As||wgIG22, wgIG, wg1-8|
|Allele class||amorphic allele - genetic evidence, loss of function allele|
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|Nature of the Allele|
|Mutations Mapped to the Genome|
|Associated Sequence Data|
|Nature of the lesion|
|Phenotype Manifest In|
All epidermal cells secrete denticles in the mutant embryo.
Embryos completely lack segment polarity and have a lawn of uniform, large, thick denticles covering the ventral epidermis. The embryos are much smaller than wild type. They are usually closed dorsally. There are only 8 rows of ventral epidermal cells per segment in wgl-8 embryos (wild-type number is, on average, 12 rows per segment). The cells are larger than normal and are cuboidal. Cells in the ventral epidermis enter mitosis 16 in mutant embryos (as occurs in wild type) and mitotic figures are as readily apparent in the ventral epidermis in stage 12 mutant embryos as they are in wild-type embryos.
Patterning defects evident in the denticle belts. Many mutant embryos are dorsally closed but exhibit severe defects in dorsal patterning, with loss of dorsal hairs and the presence of abnormal cuticular structures. A proportion show a mild dorsal-open phenotype. Leading edge cells never elongate along the DV axis, instead they stretch along the AP axis. Certain lateral cells contract like leading edge cells, stretching along the AP axis.
Posterior cells of each segment are transformed to anterior fates in homozygous embryos and secrete denticles. Most of the denticles of these embryos resemble the large type found in normal row 5. Denticle orientation is often reversed or aligned towards the ventral midline.
Homozygous embryos lack RP2 neurons.
Embryos are shorter than wild-type and secrete only denticles with no naked cuticle. wgl-8 embryos expressing armS10.Scer\UAS.T:Hsap\MYC (using Scer\GAL4e22c) produce a cuticle phenotype similar to embryos expressing armS10.Scer\UAS.T:Hsap\MYC (using Scer\GAL4e22c) in a wild-type background; nearly all secreted cuticle is naked. wgl-8 embryos expressing armΔN.Scer\UAS (using Scer\GAL4e22c) secrete naked cuticle interspersed with denticles on their ventral surface, while the dorsal surface is unchanged from the wgl-8 mutant phenotype.
Only one central invagination fold of the stomodeal invagination is observed.
Embryos exhibit a lawn of denticle belts.
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.
Defective in gonad assembly.
Mutant embryos have a lawn of row-5-type ventral denticles, with segmental polarity reversals.
hh expression in the embryo begins to fade as the germ band reaches full extension, though it does persist in a few midline cells which may be neuroblasts.
Before stage 10 wg embryos have normal hh expression, but it begins to decay at stage 10 and is gone by stage 11.
Very strong segment polarity phenotype.
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.
The RP2 neuron is the only identifiable cell altered. The restricted phenotype may be due to improper communication between neurons.
Embryos lack head cuticle and there are no or very rudimentary filzkorper. Embryos show an aberrant pattern of cell death and lack of parasegmental and segmental boundaries.
|NOT Enhancer of|
|NOT Suppressor of|
|Phenotype Manifest In|
|NOT suppressed by|
|NOT Enhancer of|
|NOT Suppressor of|
ovo[svb-108]/Y ; wg[l-8]/+ larvae raised at 25[o]C have significantly fewer quaternary trichomes compared to controls.
Loss of the second midgut constriction in wgl-8 mutant embryos is suppressed by CbydsRNA.cTa. Loss of the first midgut constriction in CbydsRNA.cTa injected embryos is partially suppressed by wgl-8.
Expression of slp1hs.PC in wgl-8 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.
Addition of W05014 or Df(3L)H99 does not result in any pronounced improvement of the wgl-8 segment polarity defect; all cells still secrete a uniform lawn of denticles and the cuticle remains smaller than wild type in double mutant embryos. However, the number of denticles is more than doubled in wgl-8 ; Df(3L)H99 embryos compared to wgl-8 single mutants, and the denticles secreted by the double mutants are much smaller than in wgl-8 single mutants. The effect of a reduction in W+ dose on wgl-8 is additive The number of rows of ventral epidermis cells is increased to 12-14 per segment in wgl-8 ; Df(3L)H99 embryos and the cells are much smaller than in wgl-8 single mutants. Most of the cells are cuboidal, they create a pattern of block-like pseudosegments and all cells secrete denticles in the double mutant embryos.
wgl-8,pucA251.1F3 double mutants show a novel loss of dorsal cuticle phenotype. Dorsal closure is never initiated. Lateral epidermal cells elongate along the AP axis and resemble leading edge cells. Massive cell degeneration is seen in the lateral and dorsal epidermis of late embryos.
|Complementation & Rescue Data|
|Stocks ( 2 )|
|Notes on Origin|
|External Crossreferences & Linkouts|
|Synonyms & Secondary IDs ( 6 )|
(Cox and Baylies, 2005, Tolwinski and Wieschaus, 2004, Bach et al., 2003, Tolwinski et al., 2003, Zhou et al., 2001, Halfon et al., 2000, Cox et al., 2000, Alcedo et al., 2000, McEwen et al., 2000, Bhat et al., 2000, Lin and Perrimon, 1999, Fuss and Hoch, 1998, Carmena et al., 1998, Loureiro and Peifer, 1998, Richter et al., 1998, Pai et al., 1997, Buratovich et al., 1997, Bhat and Schedl, 1997, van de Wetering et al., 1997, Rulifson et al., 1996, Hoch and Pankratz, 1996, Bhat, 1996, Goriely et al., 1996, Manoukian et al., 1995, Yoffe et al., 1995, Schwartz et al., 1995, Peifer et al., 1994, Pankratz and Hoch, 1995, Warrior, 1994, van den Heuvel et al., 1993, Irvine and Wieschaus, 1994, Peifer et al., 1994, van den Heuvel et al., 1993, Bejsovec and Wieschaus, 1993, Li and Noll, 1993, Li et al., 1993, Tabata et al., 1992, Lee et al., 1992, Peifer et al., 1991, Riggleman et al., 1990, Patel et al., 1989, Frasch and Levine, 1987, Perrimon and Mahowald, 1987, Estrada et al., 2006, Frankel et al., 2010, Peradziryi et al., 2011)
|Secondary FlyBase IDs|
|References ( 59 )|
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|Recent research papers ( 2 )|