FlyBase Allele Report: Dmel\Gli[AE2Δ45]

General Information

Symbol

Dmel\Gli^AE2Δ45

Species

D. melanogaster

Name

FlyBase ID

FBal0042599

Feature type

allele

Associated gene

Dmel\Gli

Associated Insertion(s)

Carried in Construct

Key Links

Genomic Maps

JBrowse

Allele class

amorphic allele - genetic evidence

Mutagen

Nature of the Allele

Allele class

amorphic allele - genetic evidence

(Auld et al., 1995)

Mutagen

Delta2-3 transposase

(Auld et al., 1995)

P-element activity

(Ashburner et al., 1999.10.12)

Progenitor genotype

Gli^AE2

(Auld and Roote, 1998.12.14, Auld et al., 1995)

Cytology

Description

Excision of the P-element and deletion of Gli sequences from point of insertion to within the intron upstream of initiator codon.

(Auld et al., 1995)

Mutations Mapped to the Genome

Curation Data

Type

Location

Additional Notes

References

deletion

2L:15,760,623..15,762,783 [-]

Comment:

deletion

(Auld et al., 1995)

Variant Molecular Consequences

Associated Sequence Data

DDBJ / EMBL / GenBank

DNA sequence

Protein sequence

UniProtKB/Swiss-Prot

UniProtKB/TrEMBL

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

lethal

(Schulte et al., 2003, Auld and Roote, 1998.12.14, Auld et al., 1995)

lethal - all die during embryonic stage

(Padash-Barmchi et al., 2010)

some die during embryonic stage

(Padash-Barmchi et al., 2010)

visible

(Schulte et al., 2003)

Phenotype Manifest In

embryonic peripheral glial cell 4

(Auld et al., 1995)

embryonic peripheral glial cell 10

(Auld et al., 1995)

epithelial cell

(Schulte et al., 2003)

intermediate peripheral glial cell of ISN

(Auld et al., 1995)

peripheral glial cell 4 of SNc

(Auld et al., 1995)

pleated septate junction

(Schulte et al., 2003)

septate junction

(Schulte et al., 2003)

Detailed Description

Statement

Reference

Gli^AE2Δ45 homozygous embryos exhibit diameter increases in their primary tracheal branches.

(Paul et al., 2003)

Epidermal cells within the abdominal segments of Gli^AE2Δ45 mutants are slightly taller and have a more uniformly columnar appearance than wild-type cells. Septate junction development, as assayed with cellular markers, appears abnormal in Gli^AE2Δ45 mutants. A number of defects in pleated septate junction (pSJ) structure are seen in the epidermis of Gli^AE2Δ45 mutant embryos; while the total number of septa at a cell-cell contact is statistically equivalent in wild-type and mutant embryos, there are more clusters containing fewer septa/cluster in the mutant embryos. pSJ defects at tricellular corners are also seen in these animals; pSJ septa are often absent at one or more bicellular contacts, in the region immediately flanking the tricellular channel (in contrast to wild type where septa are typically present at all bicellular contacts of a tricellular junction). In the Gli^AE2Δ45 mutant epidermis, large regions of delamination are observed in the basal portion of the lateral membrane domain of >30% of contacting cells, as opposed to 5% in wild-type. In addition, the gaps are of a smaller size in wild-type. Unlike wild-type, the epithelia of Gli^AE2Δ45 mutant salivary glands fail to exclude rhodamine-dextran dye injected into the hemocoel of approximately stage 17 embryos from the salivary gland lumen; the dye is able to pass between epithelial cells at multiple consecutive cell-cell contacts in the mutant embryos.

(Schulte et al., 2003)

Peripheral glia do not completely wrap the peripheral axons.

(Auld et al., 1995)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Phenotype Manifest In

Additional Comments

Genetic Interactions

Statement

Reference

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Fails to complement

Gli^dv1

(Venema et al., 2004)

Gli^dv2

(Venema et al., 2004)

Gli^dv3

(Venema et al., 2004)

Gli^dv4

(Venema et al., 2004)

Gli^dv5

(Venema et al., 2004)

Rescued by

Gli^AE2Δ45 is rescued by Gli^UAS.cPa/Scer\GAL4^da.G32

(Padash-Barmchi et al., 2010)

Gli^AE2Δ45 is rescued by Scer\GAL4^da.G32/Gli^DD.UAS

(Padash-Barmchi et al., 2010)

Gli^AE2Δ45 is rescued by Gli^FF.UAS/Scer\GAL4^da.G32

(Padash-Barmchi et al., 2010)

Partially rescued by

Gli^AE2Δ45 is partially rescued by Scer\GAL4^da.PU/Gli^UAS.cSa

(Schulte et al., 2006)

Gli^AE2Δ45 is partially rescued by Scer\GAL4^da.PU/Gli^UAS.Tag:HA

(Schulte et al., 2006)

Gli^AE2Δ45 is partially rescued by Scer\GAL4^da.PU/Gli^{ΔPDZ.UAS.Tag:HA}

(Schulte et al., 2006)

Gli^AE2Δ45 is partially rescued by Gli^UAS.cSa/Scer\GAL4^da.G32

(Schulte et al., 2003)

Not rescued by

Gli^AE2Δ45 is not rescued by Gli^UAS.cSa/Scer\GAL4^repo

(Schulte et al., 2003)

Comments

Expression of Gli^Scer\UAS.cPa under the control of Scer\GAL4^da.G32 fully rescues the embryonic lethality of Gli^AE2Δ45 mutants. Rescued embryos develop into larvae, but the majority of these become paralysed and die. Adult escapers exhibit malformed legs and fail to inflate their wings.

Expression of Gli^DD.Scer\UAS under the control of Scer\GAL4^da.G32 fully rescues the embryonic lethality of Gli^AE2Δ45 mutants. Rescued embryos develop into larvae, but the majority of these become paralysed and die. Adult escapers exhibit malformed legs and fail to inflate their wings.

Expression of Gli^FF.Scer\UAS under the control of Scer\GAL4^da.G32 fully rescues the embryonic lethality of Gli^AE2Δ45 mutants. Rescued embryos develop into larvae, but the majority of these become paralysed and die. Adult escapers exhibit malformed legs and fail to inflate their wings.

(Padash-Barmchi et al., 2010)

Expression of Gli^Scer\UAS.cSa under the control of Scer\GAL4^da.PU fully rescues the embryonic lethality of Gli^AE2Δ45 homozygotes. 58% of the rescued adults have leg defects.

Expression of Gli^{Scer\UAS.T:Ivir\HA1} under the control of Scer\GAL4^da.PU fully rescues the embryonic lethality of Gli^AE2Δ45 homozygotes. 50% of the rescued adults have leg defects.

Expression of Gli^{ΔPDZ.Scer\UAS.T:Ivir\HA1} under the control of Scer\GAL4^da.PU fully rescues the embryonic lethality of Gli^AE2Δ45 homozygotes. 100% of the rescued adults have leg defects.

(Schulte et al., 2006)

The Gli^AE2Δ45 mutant phenotype and lethality can be rescued by expression of Gli^Scer\UAS.cSa under the regulation of Scer\GAL4^da.G32. 78% of rescued embryos hatch and survive to adulthood. Rescued adults are fertile and can be maintained as a stable stock, however, 58% have severe leg defects. The metatarsus and tibia are typically bent at 45^o toward the midline, and necrotic tissue is often present on the medial aspect of the limbs and limb joints. The lethality of homozygous Gli^AE2Δ45 mutants cannot be rescued by expression of Gli^Scer\UAS.cSa under the regulation of the glial-specific driver Scer\GAL4^repo.

(Schulte et al., 2003)

Images (0)

Mutant

Wild-type

Stocks (0)

Notes on Origin

Discoverer

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (3)

Reported As

Symbol Synonym

Gli^AE2Δ45

(Byri et al., 2015, Padash-Barmchi et al., 2010)

Gli^Δ45

(Schulte et al., 2006)

gli^AE2-45

(Paul et al., 2003)

Name Synonyms

Secondary FlyBase IDs

References (9)

Report Sections

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