FB2024_03 , released June 25, 2024
Allele: Dmel\wgl-16
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General Information
Symbol
Dmel\wgl-16
Species
D. melanogaster
Name
FlyBase ID
FBal0018508
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
wgcx3
Key Links
Mutagen
Nature of the Allele
Progenitor genotype
Associated Insertion(s)
Caused by aberration
Cytology
Description

Southern blotting shows a breakpoint in the +14.6 - +16.3 interval, DNA right of +16.3 is still present demonstrating that the 3' breakpoint is not one end of a deficiency. The relationship of the wgl-16 lesion to the cytology of the Df(2L)wg-CX3 chromosome is not clear; they might be related parts of a complex rearrangement, or might be independent events in the same chromosomal region. The wgl-16 mutation is associated with an insertion of unknown DNA just 3' to the transcription unit (FBrf0046100; FBrf0066940).

Insertion of DNA in the 3' control region.

17kb insertion into the 3' regulatory region.

Deletion that brings other sequences close to the transcription terminus, thereby reducing the production of mRNA and protein.

Approximately 17kb insertion at the 3' end of the wg transcript.

Deletion of sequences between position +10.8 and +15.6 on the wg map.

break between +10.8 and 15.0 kb

Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
Variant Molecular Consequences
Associated Sequence Data
DNA sequence
Protein sequence
 
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 )
 
Disease-implicated variant(s)
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

Mutants show ectopic retinogenesis along the dorsal margin of the eye disc.

wg17en40cP1/wgl-16 flies show the loss of nearly all pseudotracheae, which are structurally characteristic of the distiproboscis. These flies show no significant loss of taste bristles nor any significant change in mediproboscis morphology.

wgl-16/wgSp-1 females have reduced vaginal plates and tergite eight and the vulva is mainly absent. wgl-16/wgSp-1 males lack the penis apparatus and most of the clasper, and the lateral plates are fused.

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

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

Dominantly enhances the appearance of an apoptotic cluster of cells in the primordial wing tip of the late third larval instar biomb-1/Y wing disc.

Most wgl-16/wgen11 flies lack antennal structures.

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

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.

25% of wgl-16/wgP flies have wings on the prothoracic segment, and the mesothoracic wings and metathoracic halteres are always absent. 10% of wgl-16/wgP flies show a varying degree of transformation of the metathoracic legs to halteres, ranging from graded removal of the distal segments (tibia and tarsus), through distortion of the femur and graded removal of leg bristles, to transformation of the coxa and trochanter into the first and second segments of the haltere.

In trans to null alleles of wg, wgl-16 gives pupal lethality, indicating wgl-16 is not a null allele of wg.

wgl-16/wgSp-1 individuals are lethal. Adult escapers lack one or both anterior dorsocentral bristles and more rarely also the posterior postalar bristle and the presutural bristle. They also exhibit loss of distal antennal segments and in rare cases exhibit antennal duplication. Individuals in combination with wgSp-revP, wgP and wgl-17 are pupal lethal. Individuals are adult viable and exhibit the wing phenotype when in combination with wg1. When in combination with wgspd-j2 individuals are lethal, escapers lack antennae and the first pair of legs.

wgl-16/wgl-12 larvae grown at the restrictive temperature result in heads that lack both the lateral and mediolateral structures causing the ocelli to be directly adjacent to the compound eyes. Ocellar cuticle and the ocelli are larger than wild type.

wgCE7/wgl-16 transheterozygotes are pupal lethal. Lethality can be suppressed by wgPE1.

Homozygotes display leg pattern element disruptions, these are also seen in the pupal lethal wgl-16/wgNZ combination.

The heteroallelic combination wgl-12/wgl-16 has been used as a temperature sensitive genotype to study the requirement for wg gene product in the development of the leg, wing and haltere imaginal discs: wg is required only during the second larval instar in the wing and haltere discs, whereas legs are affected by temperature shifts at all times up until 96 hours after egg laying (at 25oC).

Adult homeotic transformation of wing to notum.

pupal lethal

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Suppressed by
Statement
Reference
Suppressor of
Statement
Reference

wg[+]/wgl-16 is a suppressor of lethal | somatic clone | pupal stage phenotype of Stat92E85C9

Phenotype Manifest In
Suppressed by
Enhancer of
Statement
Reference

wg[+]/wgl-16 is an enhancer of wing disc phenotype of biomb-1

Suppressor of
Statement
Reference

wg[+]/wgl-16 is a suppressor of eye | somatic clone phenotype of Stat92E85C9

wg[+]/wgl-16 is a suppressor of cuticle & adult external head | somatic clone phenotype of Stat92E85C9

wg[+]/wgl-16 is a suppressor of head | somatic clone phenotype of Stat92E85C9

wgl-16 is a suppressor of arista | increased number phenotype of obk1

Other
Additional Comments
Genetic Interactions
Statement
Reference

Flies carrying Stat92E85C9 Minute clones in a wgl-16/+ background show a significantly increased rate of eclosion compared to those with a wild-type background. Further, eclosed wgl-16/+; Stat92E85C9 Minute flies show less severe phenotypes compared to eclosed Stat92E85C9 Minute flies.

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 antenna phenotype of wgl-16/wgen11 flies is significantly rescued by fz3G10.

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

The third leg discs of wgl-16 l(2)gd11 homozygous larvae display an overgrowth phenotype but not duplicate discs.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Fails to complement
Partially rescued by
Comments

Expression of wgScer\UAS.cLa under the control of Scer\GAL4cad-em459 in wgl-16/wgSp-1 females sometimes results in recovery of the vaginal plates and tergite eight, but not the vulva. The analia are much reduced in some cases and some females have no genital and anal structures. Expression of wgScer\UAS.cLa under the control of Scer\GAL4cad-em459 in wgl-16/wgSp-1 males results in recovery of genital structures such as the claspers and penis apparatus, although the penis apparatus is sometimes still reduced. Analia are almost normal or reduced.

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

Baker.

Comments
Comments

There is enough wg activity in homozygotes to produce imaginal discs but not enough for normal disc development.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (4)
References (41)