Polytene chromosomes normal.
A 2416 bp deletion in the 3' enhancer region of wg.
Small deletion in the 3' untranslated region (UTR).
Insertion downstream of coding region.
Approximately 2.5kb deletion at the 3' end of the wg transcript.
Small deficiency extending from the interval +16.8 to +17.1 on the wg map off to the right.
deletion from +16.8 to +17.1 kb
A 2416 bp deletion in the 3' enhancer region of wg, starting coordinate 2L:7324252 (Release 5 coordinates). See also Fig. S1.
mesonotum | ectopic (with wg17en40cP1)
terminal bouton | larval stage (with wgGBM)
wing (with wg17en40cP1)
wing disc (with wg17en40cP1)
In a significant proportion of wg1 homozygotes, adults show transformation of one or both wings into notum and third instar larvae present wing discs with presumptive wing tissue replaced by notum tissue; these adults also present decreased wing regeneration capacity, as shown by the significant decrease in the number of adults with fully regenerated wings following rpr-induced damage to the third instar wing disc pouch, as compared to wild-type controls.
A minority of wg1/+ flies have at least one wing transformed into notum.
Homozygous wg1 larvae do not show the increase in ghost bouton formation seen in controls upon spaced 5X K[+] depolarisation.
Homozygotes show a wing to notum transformation.
wg1/wg17en40cP1 wing discs show replacement of wing by a duplication of notum structures, which is also seen in the adult flies.
Flies often lack wings and show a symmetric duplication of body wall structures.
Semiviable, deletion of the ventralmost part of the eye. Ectopic furrow movement initiates predominantly from the ventral margin.
Additional bristles present on the second leg.
Flies exhibit a variable loss of one or two wings.
Adult homeotic transformation of wing to notum.
Phenotype shows incomplete penetrance and expressivity; 50.8% of flies have no wings, 40.67% have one wing, and 8.47% have two wings.
viable
wg1 has visible | adult stage | dominant phenotype, enhanceable by p53[+]/p53-ns
wg1 has visible | adult stage | dominant phenotype, enhanceable by p53[+]/p5311-1B-1
wg1 has visible | adult stage | dominant phenotype, enhanceable by p535A-1-4/p53[+]
wg1 has abnormal neuroanatomy | larval stage phenotype, non-enhanceable by eghUAS.Tag:MYC/Scer\GAL4nSyb.PS
wg1/wgGBM has abnormal neuroanatomy | larval stage phenotype, non-enhanceable by eghUAS.Tag:MYC/Scer\GAL4nSyb.PS
wg1/wgl-17 has visible phenotype, suppressible by HipkUAS.Tag:HA/Scer\GAL469B
wg1/wgGBM has abnormal neuroanatomy | larval stage phenotype, non-suppressible by eghUAS.Tag:MYC/Scer\GAL4nSyb.PS
wg1 has abnormal neuroanatomy | larval stage phenotype, non-suppressible by eghUAS.Tag:MYC/Scer\GAL4nSyb.PS
wg1 is a non-enhancer of visible phenotype of upd1GMR.PB
wg1/wg[+] is a suppressor | partially of visible | adult stage phenotype of CtBP87De-10, Scer\GAL4rn-GAL4-5, egrUAS.cUa
wg1/wg[+] is a suppressor | partially of short lived phenotype of Hsap\HTTQ93.ex1.UAS, Scer\GAL4elav.PU
wg1 is a non-suppressor of visible phenotype of upd1GMR.PB
egh[+]/egh62d18, wg1 has abnormal neuroanatomy | larval stage phenotype
wg1 has embryonic/larval neuromuscular junction phenotype, non-enhanceable by eghUAS.Tag:MYC/Scer\GAL4nSyb.PS
wg1 has terminal bouton | larval stage phenotype, non-enhanceable by eghUAS.Tag:MYC/Scer\GAL4nSyb.PS
wg1/wgGBM has embryonic/larval neuromuscular junction phenotype, non-enhanceable by eghUAS.Tag:MYC/Scer\GAL4nSyb.PS
wg1/wgGBM has terminal bouton | larval stage phenotype, non-enhanceable by eghUAS.Tag:MYC/Scer\GAL4nSyb.PS
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
wg1/wgGBM has embryonic/larval neuromuscular junction phenotype, non-suppressible by eghUAS.Tag:MYC/Scer\GAL4nSyb.PS
wg1/wgGBM has terminal bouton | larval stage phenotype, non-suppressible by eghUAS.Tag:MYC/Scer\GAL4nSyb.PS
wg1 has embryonic/larval neuromuscular junction phenotype, non-suppressible by eghUAS.Tag:MYC/Scer\GAL4nSyb.PS
wg1 has terminal bouton | larval stage phenotype, non-suppressible by eghUAS.Tag:MYC/Scer\GAL4nSyb.PS
wg1 is a non-enhancer of interommatidial bristle | pupal stage phenotype of exMGH1
wg1 is a non-enhancer of eye phenotype of upd1GMR.PB
wg1/wg[+] is a suppressor | partially of wing | ectopic phenotype of CtBP87De-10, Scer\GAL4rn-GAL4-5, egrUAS.cUa
wg1 is a suppressor | partially of eye | somatic clone phenotype of exMGH1
wg1 is a suppressor | partially of eye disc | pupal stage phenotype of exMGH1
wg1 is a suppressor of pigment cell phenotype of sgl05007, wa
wg1 is a non-suppressor of eye phenotype of upd1GMR.PB
egh[+]/egh62d18, wg1 has embryonic/larval neuromuscular junction phenotype
egh[+]/egh62d18, wg1 has terminal bouton | larval stage phenotype
Expression of egrUAS.cUa under the control of Scer\GAL4rn-GAL4-5 (with tub-Gal80[ts] restricting expression to third instar larvae) in wg1/+ background does not lead to ectopic wings compared to controls.
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 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. The wingless phenotype of wg1 homozygotes is dominantly enhanced by ap78j; no wing blade is formed at approximately 90% of presumptive wing-blade-forming sites. This phenotype is partially suppressed by fz3G10.
wg1/+ significantly partially suppresses the decreased lifespan seen in flies with expression of Hsap\HTTQ93.ex1p.Scer\UAS driven by Scer\GAL4elav.PU.
Sharma.
A genotypically wg1 mutant hemithorax is usually also phenotypically mutant in gynandromorphs; thus wg1 is disc-autonomous.
Pairwise complementation analysis of wg1, wgl-8, wgH and an allele of spd reveals a complex complementation pattern.
wg function during second larval instar affected.
FlyBase curator comment: the wg1 mutation is reported as being caused by ethyl methanesulfonate in this reference but in FBrf0096285, a reference by the same author in the same issue of D.I. S., the mutation is reported as being X-ray-induced.