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General Information
Symbol
Dmel\ovoD1
Species
D. melanogaster
Name
FlyBase ID
FBal0013375
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
ovoD, Fs(1)K1237
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
point mutation
Nucleotide change:

A5064663T

Reported nucleotide change:

A1282T

Amino acid change:

K208M | ovo-PB; K79M | ovo-PC; K208M | ovo-PE

Reported amino acid change:

K79M

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

Mutation creates a new in frame AUG codon in the open reading frame in exon 2.

Nucleotide substitution: A1282T.

Amino acid replacement: K79M.

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 )
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

The pH of the fecal output of mutant females is more similar to that of wild-type virgin males than to that of wild-type virgin females.

Wild-type mated females often excrete fecal deposits which are extremely concentrated, referred to as reproductive oblong deposits (RODs), compared to the fecal deposits of wild-type males and wild-type virgin females. Mated ovoD1 females show reduced ROD production compared to wild-type mated females.

Ovaries from heterozygous ovoD1 females produce only very rarely egg chambers, which then only survive until stages 2-3 of oogenesis.

ovoD1 flies feed more than control flies. This is because they increase the volume of intake per proboscis extension, rather than by feeding at a greater frequency.

ovoD1 mutant germ lines exhibit growth arrest after stage 4 resulting in small stage 6 egg chambers, which later degenerate.

Heterozygous females have an extended life-span compared to controls.

Heterozygous adult females have atrophied ovaries containing some germ cells but lacking vitellogenic egg chambers. Wild-type clones made in the ovaries of a ovoD1 female, are significantly larger than clones of heterozygous mutant cells. This size difference is greater in clones initiated at 48 hours after egg laying (AEL) than 2 hours AEL.

The frequency of gypsy insertion into the ovo locus in a flam permissive background is higher in ovoD1/+ females than in wild-type females. gypsy insertions in ovoD1 females occur during most stages of germ-line development, in contrast to wild-type females where insertions occur only in late stages.

Heterozygous females have small ovaries bearing only early egg chambers.

Oogenesis stops at about stage 4 in heterozygous females.

Females carrying ovoD1 in a wild-type or ovo-/+ background show dominant female sterility. Heterozygous females contain no mature eggs.

In heterozygous females oogenesis is arrested prior to or at stage 4.

Oogenesis in heterozygous females is mainly arrested prior to stage 4.

Germ-cell arrest.

Heterozygous females do not lay eggs, egg chambers form but degenerate before vitellogenic stages.

The egg chambers of heterozygous females fail to initiate vitellogenesis, and no eggs are laid. The soma is wild-type. Females heterozygous for both ovoD1 and snf1 have germ cells with a male-like morphology.

Mutant gene activity works in opposition to wild type activity. Viable. Male germ line is fertile, female germ line has no vitellogenic egg chambers.

The presence of ovoD1 has no effect on the dl1 phenotype.

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

ovoD1 has long lived | dominant phenotype, non-enhanceable by chico1

NOT Enhancer of
Statement
Reference

ovoD1 is a non-enhancer of long lived | dominant phenotype of chico1

Suppressor of
Statement
Reference
Phenotype Manifest In
Suppressor of
Statement
Reference

ovoD1 is a suppressor of epithelium | somatic clone phenotype of sqhAX3

Additional Comments
Genetic Interactions
Statement
Reference

Wild-type mated females often excrete fecal deposits which are extremely concentrated, referred to as reproductive oblong deposits (RODs), compared to the fecal deposits of wild-type males and wild-type virgin females. ovoD1 females which have been mated to Acp70A0/Df(3L)Δ130 males do not produce RODs.

The deleterious effect on female lifespan of expression of EcRB1-ΔC655.W650A.Scer\UAS under the control of Scer\GAL4da.Switch.PT in the presence of RU486 is suppressed by ovoD1.

The deleterious effect on female lifespan of expression of EcRB1-ΔC655.F645A.Scer\UAS under the control of Scer\GAL4da.Switch.PT in the presence of RU486 is suppressed by ovoD1.

The deleterious effect on female lifespan of expression of EcRdsRNA.Scer\UAS.cCa under the control of Scer\GAL4da.Switch.PT in the presence of RU486 is partially suppressed by ovoD1.

sqhAX3 follicle cell clones maintain their rectangular shape when cyst growth is blocked in ovoD1 mutants, whereas sqhAX3 cells are deformed when the cyst grows. The cyst bulges out underneath the sqhAX3 clones only in the wild-type background, not in ovoD1 mutant cysts.

ovoD1 chico1 double heterozygotes live as long as chico1/+ single heterozygotes and significantly longer than ovoD1/+ single heterozygotes.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Not rescued by
Comments

ovoS-7.2 cannot rescue the sterility of heterozygous females.

Images (0)
Mutant
Wild-type
Stocks (4)
Notes on Origin
Discoverer
Comments
Comments

The dominant ovoD1 mutation has been reverted to a recessive loss of function mutation by insertion of a gypsy element.

The ovoD1 allele has been cloned and transposed to several regions of the genome in P element vectors to facilitate the generation of germ line mosaics for autosomal mutations.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (7)
References (60)