FB2025_05 , released December 11, 2025
Allele: Dmel\Ilk1
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General Information
Symbol
Dmel\Ilk1
Species
D. melanogaster
Name
FlyBase ID
FBal0031864
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
l(3)78Ca1
Key Links
Genomic Maps

Nature of the Allele
Progenitor genotype
Cytology
Description

Amino acid replacement: W211term.

Nucleotide substitution: G?A.

Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
Nucleotide change:

G21218167A

Reported nucleotide change:

G?A

Amino acid change:

W211term | Ilk-PA

Reported amino acid change:

W211term

Comment:

G to A nucleotide change at the second or third position of the Trp codon leads to a nonsense mutation. (exact site of mutation unspecified)

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

Ilk1/+ does not significantly affect resistance to ethanol-induced sedation.

Adult-generated Ilk1 homozygous mutant intestinal stem cell clones have reduced maintenance 7 days and 14 days after clone induction compared to control clones; cells in the remaining clones are either diploid cells or immature enterocytes.

Ilk1 dorsal branch terminal cell clones do not cause any detectable defects in terminal cell morphology.

Homozygotes die at the end of embryogenesis. The cuticle is completely normal in Ilk1/Df(3L)Pc-14d embryos. Midgut development is normal in mutant embryos. Stage 17 homozygous and Ilk1/Df(3L)Pc-14d embryos show defects in most of the muscles, with actin clumped together rather than extending along the length of the muscles as in wild type. Muscles where the actin has detached from the plasma membrane and the membrane remains attached at its normal position adjacent to the extracellular matrix are seen in Ilk1/Df(3L)Pc-14d embryos. Muscles where both the plasma membrane and actin have retracted are also seen, although they are still separate. Homozygous embryos derived from homozygous female germline clones (lacking both maternal and zygotic Ilk function) have a modestly more severe phenotype than homozygous embryos (lacking zygotic Ilk function); they show clumping of actin in the muscles slightly earlier, at stage 16. These embryos have normal cuticles. Homozygous clones in the wing result in a wing blister. Wing blisters are associated with clones on either side of the wing blade.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Suppressor of
Statement
Reference
Phenotype Manifest In
Additional Comments
Genetic Interactions
Statement
Reference

Ilk1/+ significantly suppresses (to wild type levels) the increased resistance to ethanol-induced sedation seen in flies with expression of icsdsRNA.Scer\UAS.WIZ driven by Scer\GAL4elav.PU.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Fails to complement
Comments
Images (0)
Mutant
Wild-type
Stocks (2)
Notes on Origin
Discoverer

A.T.C. Carpenter.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (4)
References (15)