FB2026_01 , released March 12, 2026
FB2026_01 , released March 12, 2026
Allele: Dmel\zip3
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General Information
Symbol
Dmel\zip3
Species
D. melanogaster
Name
FlyBase ID
FBal0263483
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Key Links
Genomic Maps

Allele class
Nature of the Allele
Allele class
Progenitor genotype
Cytology
Description

Amino acid replacement: Q1076term.

The mutation results in a truncated protein that lacks part of the coiled coil domain.

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

C24994920T

Amino acid change:

Q1076term | zip-PA; Q1031term | zip-PB; Q991term | zip-PC; Q1036term | zip-PD; Q991term | zip-PE; Q999term | zip-PF; Q991term | zip-PG; Q999term | zip-PH; Q1044term | zip-PI

Reported amino acid change:

Q1076term

Comment:

Site of nucleotide substitution in mutant inferred by FlyBase based on reported amino acid change.

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

zip3 homozygous mutants show laterality defects in the proventriculus and anterior midgut. The laterality of the other parts of the embryonic gut, including the hindgut and the posterior part of the midgut is normal in these mutants. The proventriculus and the anterior midgut do not rotate (as in wild-type) in these mutants at stages 15 to 17.

zip3 heterozygotes appear wild-type.

zip3/zip4 embryos show laterality defects in the proventriculus and anterior midgut. The laterality of the other parts of the embryonic gut, including the hindgut and the posterior part of the midgut is normal in these mutants. The proventriculus and the anterior midgut do not rotate (as in wild-type) in these mutants at stages 15 to 17.

zip3/zip1 embryos show laterality defects in the proventriculus and anterior midgut. The laterality of the other parts of the embryonic gut, including the hindgut and the posterior part of the midgut is normal in these mutants. The proventriculus and the anterior midgut do not rotate (as in wild-type) in these mutants at stages 15 to 17.

zip3/zip2 embryos show laterality defects in the proventriculus and anterior midgut. The laterality of the other parts of the embryonic gut, including the hindgut and the posterior part of the midgut is normal in these mutants. The proventriculus and the anterior midgut do not rotate (as in wild-type) in these mutants at stages 15 to 17.

zip3/Df(2R)gsb embryos show laterality defects in the proventriculus and anterior midgut. The laterality of the other parts of the embryonic gut, including the hindgut and the posterior part of the midgut is normal in these mutants. The proventriculus and the anterior midgut do not rotate (as in wild-type) in these mutants at stages 15 to 17.

Approximately 20% of zip3 stage 17 embryos show left-right inversion of looping of the esophagus.

zip3 mutants exhibit dorsal closure defects.

Differentiation and development of the trunk visceral mesoderm appears normal in stage 12 zip3 homozygous embryos.

The circular visceral muscle appears to be correctly differentiated and migrates normally in stage 16 zip3 homozygotes.

Examination of the actin cytoskeleton through expression of MoeScer\UAS.T:Avic\GFP under the control of Scer\GAL4NetB-NP1522) shows that the structure and closure of the midgut in zip3 stage 15 and 16 embryos is comparable to controls.

The right side specific rearrangement of the circular visceral muscle cells is abolished in zip3 stage 15-16 embryos.

The rotation of the ventral midline of the circular visceral muscle cells relative to the midline of the embryo that is seen in wild type does not occur in stage 16 zip3 embryos.

The posterior migration of the ventral anterior midgut epithelium (examined using MoeScer\UAS.T:Avic\GFP and Disc\RFPDsRedT4.Scer\UAS.T:nls5 under the control of the Scer\GAL448Y driver) occurs normally in early stage 16 zip3 mutants compared to controls. The movement of the anterior midgut that normally occurs at late stage 16 is disrupted in zip3 homozygotes with the posterior movement, rightward movement of the anterior region and leftward movement of the posterior region of the anterior midgut all affected.

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

A chic221 heterozygous background enhances the loss of rotation in the proventriculus and anterior midgut seen in zip3 homozygotes.

A zip3 heterozygous background enhances the loss of rotation in the proventriculus and anterior midgut seen in sqhAX3/Y mutants.

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

zipScer\UAS.T:Avic\GFP driven by Scer\GAL4da.G32 rescues the loss of rotation in the proventriculus and anterior midgut seen in zip3 homozygotes.

zipScer\UAS.T:Avic\GFP driven by the circular visceral muscle drivers Scer\GAL4how-24B, Scer\GAL4Gap1-NP3392, Scer\GAL448Y or Scer\GAL4NetB-NP1522 partially rescues the loss of rotation in the proventriculus and anterior midgut seen in zip3 homozygotes.

zipScer\UAS.T:Avic\GFP driven by the longitudinal visceral muscle drivers Scer\GAL4NP221 or Scer\GAL4tey-5053A fails to rescue the loss of rotation in the proventriculus and anterior midgut seen in zip3 homozygotes.

zipScer\UAS.T:Avic\GFP driven by the drivers Scer\GAL4NP5021, Scer\GAL4drm.7.1, Scer\GAL4byn-Gal4, Scer\GAL4elav-C155 or Scer\GAL4wg.PM fails to rescue the loss of rotation in the proventriculus and anterior midgut seen in zip3 homozygotes.

Expression of zipScer\UAS.T:Avic\GFP driven by Scer\GAL4wg.PM suppresses the dorsal closure defects in zip3 homozygotes although the no rotation phenotype is not suppressed.

Expression of zipScer\UAS.T:Avic\GFP continuously in a non-permissive temperature (32[o]C), under the control of Scer\GAL4da.G32 and Scer\GAL80ts.αTub84B, rescues the laterality defects found in zip3 mutants. The zip3 rotation defects are not rescued when the 1 hour shift to the non-permissive temperature occurs from stage 14 onwards. The temperature shift applied from 16 to 17 hours after egg laying (AEL), which corresponds to stage 12, leads to the most efficient rescue of the laterality defects associated with zip3 mutants. However, expression of zipScer\UAS.T:Avic\GFP after 22 hours AEL, corresponding to stage 14, does not rescue the laterality, 'no rotation' phenotype.

zipScer\UAS.T:Avic\GFP driven by Scer\GAL4how-24B partially rescues the loss of side specific rearrangement in circular visceral muscle cells seen in zip3 homozygotes. The failure of the circular visceral muscle midline to rotate in relation to the midline of the embryo is also partially rescued.

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Synonyms and Secondary IDs (1)
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    References (1)