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General Information
D. melanogaster
FlyBase ID
Feature type
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
Allele class
Nature of the Allele
Allele class
Mutations Mapped to the Genome
Additional Notes

Two bases (TT) are deleted.

Associated Sequence Data
DNA sequence
Protein sequence
Progenitor genotype
Nature of the lesion

Deletion of two T-A base pairs out of the six from 2258 to 2263 (coordinates relative to accession number AF144092), resulting in a predicted frameshift that causes a truncation after residue 726.

No mutations are detected in the open reading frame of mus201D1 mutants (it remains possible that this mutation is a mutation in the promoter region).

Expression Data
Reporter Expression
Additional Information
Marker for
Reflects expression of
Reporter construct used in assay
Human Disease Associations
Disease Ontology (DO) Annotations
Models Based on Experimental Evidence ( 0 )
Modifiers Based on Experimental Evidence ( 1 )
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description

Exposure of mus201D1 mutant larvae to DDVP for 48 hours results in a significant increase in the migration of DNA in midgut cells at 0.15, 1.5 and 15ng/ml concentrations of DDVP as compared to controls.

mus201D1 mutants have a similar frequency of single-strand annealing repair (SSA) compared to controls in a P{wIw.FRT} hemizygous assay to study DNA double-stranded break repair when assayed at 32oC or 38oC.

When homozygous mutants are UV irradiated a complete ablation of the eye is seen due to an increase in apoptotic cell death. Light-induced photorepair partially rescues the eye phenotype.

UVA irradiation (at 320-400nm) is mutagenic in mus201D1 mutants, as in wild-type. mus201D1 mutants are 10-fold more sensitive than the wild-type to UVC (200-280nm) damage. Irradiation with 310nm UVB is 24 times more mutagenic in mus201D1 mutants than in controls, 14 times more mutagenic at 320nm and 1.7 times more at 340nm, respectively.

A high frequency of genomic damage (measured by arbitrarily primed PCR fingerprinting) is induced in mus201D1 males after exposure to 2-AAF compared to wild-type flies.

Homozygotes are hypersensitive to methyl methanesulfonate compared to wild-type flies.

A higher frequency of sex linked recessive lethal mutations are induced by acrolein in a mus201D1 maternal background than in a wild-type background. The hypermutability index for mus201D1 is 2.59.

Excision repair capacity is deficient and post-replication repair capacity is normal.

Mutations exhibit an absolute deficiency in the capacity to excise UV-induced pyrimidine dimers.

Flies are not ether-sensitive. Flies are hypersensitive to killing by γ-rays.

Approximately 72% of embryos hatch. Approximately 18% of mus201D1 mei-9A1 double mutant embryos hatch. Homozygous larvae derived from homozygous mothers are more sensitive to methyl methanesulfonate than homozygous larvae derived from heterozygous mothers, indicating that this mutation has a maternal effect. Homozygous larvae derived from homozygous mothers are 31.9 times more sensitive to methyl methanesulfonate and 6.6 times more sensitive to UV light than wild-type. Homozygous mus201D1 or mei-9A1 mus201D1 embryonic cells in culture show no detectable unscheduled DNA synthesis (UDS) activity in response to methyl methanesulfonate, N-methyl-N-nitrosourea or UV light, over dose ranges in which wild-type cells show a strong dose-dependent UDS response. Homozygous mus201D1 embryonic cells in culture show a reduced, but dose-dependent UDS response to X rays over a dose range in which wild-type cells show a strong dose-dependent UDS response, while mei-9A1 mus201D1 embryonic cells in culture show no detectable UDS response to X rays in the same dose range.

Hypersensitive to exposure to methyl methanesulfonate, ultraviolet light and nitrogen mustard; weakly sensitive to X rays. mus201D1 is less sensitive to nitrogen mustard and X rays than mus201A1. Homozygotes show no detectable excision repair; DNA synthetic capacity in the absence of a mutagen and repair of single-strand breaks induced by X rays is normal.

External Data
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Phenotype Manifest In
Enhanced by

mus201D1 has eye | conditional phenotype, enhanceable by p5311-1B-1

Enhancer of

mus201D1 is an enhancer of eye | conditional phenotype of p5311-1B-1

Additional Comments
Genetic Interactions

p5311-1B-1, mus201D1 double heterozygotes exhibit an enhanced retinal sensitivity to UV light and an increase in apoptotic cell death.

Viable in double homozygous combination with mus205B1, mus208B1 or mus210B1. mus205B1 mus201D1 double mutant larvae are no more sensitive to methyl methanesulfonate (MMS) than mus205B1 single mutant larvae. mus201D1 shows a fairly strong synergistic interaction with respect to sensitivity to methanesulfonate (MMS) in combination with either mus208B1 or mus210B1.

Xenogenetic Interactions
Complementation and Rescue Data
Images (0)
Stocks (3)
Notes on Origin

Homozygotes have normal postreplication repair capabilities, but excision repair is reduced to undetectable levels. Homozygous cultured cells respond to UV irradiation with normal reductions in thymidine incorporation and with the synthesis of normal-length nascent DNA.

mus201D1 does not significantly affect male or female fertility, fourth or X chromosome nondisjunction in females or X chromosome recombination in females.

An endonuclease activity which is specific for partially depurinated DNA is reduced in extracts of mus201D1 larval brain ganglia compared to wild-type.

mus201D1 has no detectable effect on the recovery of chromosomes undergoing P-element transposition.

External Crossreferences and Linkouts ( 1 )
GenBank Nucleotide - A collection of sequences from several sources, including GenBank, RefSeq, TPA, and PDB.
Synonyms and Secondary IDs (4)
References (31)