FB2026_02 , released June 18, 2026
Allele: Dmel\mre11Δ35K1
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General Information
Symbol
Dmel\mre11Δ35K1
Species
D. melanogaster
Name
FlyBase ID
FBal0175582
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
mre11-
Key Links
Nature of the Allele
Progenitor genotype
Cytology
Description

Deletion of the entire mre11 coding region.

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

mre11Δ35K1 third instar larvae exposed to 10 Gy ionizing radiation exhibit a G2/M cell cycle checkpoint defect in wing and eye discs when compared to controls.

Telomeric fusions in mre11Δ35K1 mutants result in chromosome bridges during mitosis. Approximately 3.5% of mitotic nuclei taken from 11-s instar larvae display bridges, and 12.9% of mitotic nuclei taken from 6 third instar larvae do so. This suggests that the loss of the telomere protection function of maternal mre11 happens mainly during the third instar stage.

mre11Δ35K1 homozygous or transheterozygous for mre11Δ35K1/mre1158S are viable and recovered at a Mendelian ratio.

mre11Δ35K1 mutant cells exhibit DNA breaks and telomere fusions in metaphase and anaphase.

Mutant larvae show a normal checkpoint response (a steep decline in the number of G2 cells entering mitosis) in response to irradiation with 4000 rad of X rays, but they are unable to block mitotic entry when irradiated with 500 rad. Mutant cells are highly defective in repairing chromosome breaks induced by X rays. Mutant nuclei irradiated with 500 rad display fragmented mitotic chromosomes beyond recognition.

Dividing neuroblasts in the brains of third instar mutant larvae show a number of defects. The most prominent defect is end-to-end association (telomere attachment) of chromosomes. Single telomere attachments (both between sister chromatids and between non-sister chromatids) and double telomere attachments are seen. In addition, chromosome breaks and aneuploid nuclei are seen. Chromosome bridges are often seen.

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

mre11Δ35K1 p53unspecified double mutants show the same checkpoint phenotype as mre11Δ35K1 single mutants; they show a normal checkpoint response to irradiation with 4000 rad of X rays, but they are unable to block mitotic entry when irradiated with 500 rad.

tefustg mre11Δ35K1 double homozygotes die as late third instar larvae. Double mutants do not show an additive effect on the frequency of telomere attachments and chromosome breaks in third larval instar neuroblasts.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments

The presence of mre1158S rescues the viability of mre11Δ35K1 homozygotes, although the surviving females are sterile.

Images (0)
Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (4)
Reported As
Name Synonyms
Secondary FlyBase IDs
    References (8)