FB2026_01 , released March 12, 2026
FB2026_01 , released March 12, 2026
Allele: Dmel\pcx3
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General Information
Symbol
Dmel\pcx3
Species
D. melanogaster
Name
FlyBase ID
FBal0013629
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Key Links
Genomic Maps

Nature of the Allele
Progenitor genotype
Cytology
Description

Nucleotide substitution: G?A.

Amino acid replacement: W2030term.

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

G2232264A

Reported nucleotide change:

G?A

Amino acid change:

W2030term | pcx-PC; W2034term | pcx-PE; W2030term | pcx-PF

Reported amino acid change:

W2030term

Comment:

TGG to TGA change in the W2030 codon.

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

Mutant embryos lacking both maternal and zygotic pcx function show a neurogenic phenotype. This phenotype can be paternally rescued in 80% of embryos.

The endoplasmic reticulum (ER) appears to be normal in mutant embryos lacking both maternal and zygotic pcx at stage 5. However, ER defects are apparent at stage 9 in these embryos, and enlarged ER is seen at stage 14, predominantly in the region corresponding to the dorsal epidermis of wild-type embryos at this stage.

Embryonic defects detectable during blastoderm stage.

Homozygous females lay eggs that fail to hatch.

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

Expression of NΔECN.hs in pcx3 embryos which lack maternal and zygotic pcx function partially rescues the neurogenic phenotype is 90% of embryos, while the phenotype is not rescued in the remaining 10% of embryos.

Expression of NICN.Scer\UAS under the control of Scer\GAL4arm.PS in pcx3 embryos which lack maternal and zygotic pcx function partially rescues the neurogenic phenotype: 44% of embryos are rescued, 48% are partially rescued and 8% are not rescued. The endoplasmic reticulum defects are also rescued.

Expression of Xbp1Scer\UAS.RB under the control of Scer\GAL4arm.PS in pcx3 embryos which lack maternal and zygotic pcx function partially rescues the neurogenic phenotype: 31% of embryos are fully rescued, 43% are partially rescued and 26% are not rescued. The endoplasmic reticulum defects are also rescued in 74% of cases.

Expression of Hsc70-3Scer\UAS.cEa under the control of Scer\GAL4arm.PS in pcx3 embryos which lack maternal and zygotic pcx function partially rescues the neurogenic phenotype: 67% of embryos are partially rescued and 33% are not rescued.

Expression of Hsc70-3K97S.Scer\UAS under the control of Scer\GAL4arm.PS in pcx3 embryos which lack maternal and zygotic pcx function partially rescues the neurogenic phenotype: 29% of embryos are fully rescued, 38% are partially rescued and 33% are not rescued. The endoplasmic reticulum defects are also rescued in 67% of cases.

Expression of O-fut1Scer\UAS.cSa under the control of Scer\GAL4arm.PS in pcx3 embryos which lack maternal and zygotic pcx function rescues the neurogenic phenotype and endoplasmic reticulum defects in 31% of cases.

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

Expression of pcxScer\UAS.T:Avic\GFP-EGFP under the control of Scer\GAL4arm.PS rescues the neurogenic phenotype seen in pcx3 embryos which lack maternal and zygotic pcx function (73% of embryos are rescued). The endoplasmic reticulum defects are also rescued.

In pcx3 embryos which lack maternal and zygotic pcx function, clones of cells expressing pcxScer\UAS.T:Avic\GFP-EGFP under the control of Scer\GAL4Act5C.PT do not assume a neural fate, while the surrounding cells become neurons.

Images (0)
Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer

Mohler.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (3)
Reported As
Name Synonyms
Secondary FlyBase IDs
    References (5)