Mutation creates a new in frame AUG codon in the open reading frame in exon 2.
Nucleotide substitution: A1282T.
Amino acid replacement: K79M.
A5064663T
A1282T
K208M | ovo-PB; K79M | ovo-PC; K208M | ovo-PE
K79M
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.
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.
Mutant gene activity works in opposition to wild type activity. Viable. Male germ line is fertile, female germ line has no vitellogenic egg chambers.
ovoD1 has long lived | dominant phenotype, non-enhanceable by chico1
ovoD1 is a non-enhancer of long lived | dominant phenotype of chico1
ovoD1 is a suppressor of abnormal cell shape | somatic clone phenotype of sqhAX3
ovoD1 is a suppressor of abnormal cytokinesis | somatic clone phenotype of sqhAX3
ovoD1 is a suppressor of epithelium | somatic clone phenotype of sqhAX3
ovoD1 is a suppressor of follicle cell | somatic clone phenotype of sqhAX3
ovoD1 is a suppressor of egg chamber | somatic clone phenotype of sqhAX3
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.
ovoS-7.2 cannot rescue the sterility of heterozygous females.
Komitopoulou.
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.
Parental strain: fs(1)A273.