FB2024_03 , released June 25, 2024
Allele: Dmel\Pif1167
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General Information
Symbol
Dmel\Pif1167
Species
D. melanogaster
Name
FlyBase ID
FBal0325580
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Key Links
Allele class
Nature of the Allele
Allele class
Cytology
Description

A 1.7-kb deletion within Pif1.

1695bp deletion that removes the Pif1 helicase domain. Generated by imprecise excision of P{EPgy2}CG3238EY10295.

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

Pif1167 homozygotes show increased mortality to some chemicals that induce DNA replication stress: moderate sensitivity to hydroxyurea and mild sensitivity to methyl methanesulfonate and bleomycin, but no sensitivity to paraquat, topotecan or nitrogen mustard.

Embryos derived from Pif1167 homozygous mothers rarely hatch and develop more slowly. During early development (1-2h of development at 25[o]C), these embryos show defective nuclear divisions: nuclear fallout (fully prevalent), chromosome clumping (highly prevalent), anaphase bridges and asynchronous divisions. However, there is no statistically significant increase in meiotic defects (i.e. X chromosome nondisjunction).

Pif1167 individuals do not show significant DNA repair defects in P{w[α]} assays: slight decrease in homologous recombination events and unchanged incomplete homologous recombination events that terminate via end joining, as compared to controls.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
NOT Enhanced by
NOT suppressed by
Enhancer of
Statement
Reference

Pif1167 is an enhancer of abnormal DNA repair phenotype of PolD3L2

NOT Enhancer of
Statement
Reference
NOT Suppressor of
Statement
Reference
Other
Phenotype Manifest In
Additional Comments
Genetic Interactions
Statement
Reference

Pol32L2, Pif1167 double mutants show more pronounced DNA repair defects in a P{w[α]} assay than Pol32L2 single mutants: more severely decreased homologous recombination events than Pol32L2 and increased incomplete homologous recombination events that terminate via end joining, as compared to wild-type controls.

Pif1167, DNApol-ζ3B individuals do not show significant DNA repair defects in P{w[α]} assays: slight decrease in homologous recombination events and unchanged incomplete homologous recombination events that terminate via end joining, as compared to controls.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments
Images (0)
Mutant
Wild-type
Stocks (0)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (2)
Reported As
Name Synonyms
Secondary FlyBase IDs
    References (3)