Mutation creates a new in-frame AUG codon in the open reading frame in exon 2.
Nucleotide substitution: G1572A.
Amino acid replacement: V176M.
G5064953A
G1572A
V305M | ovo-PB; V176M | ovo-PC; V305M | ovo-PE
V176M
The dominant ovoD2 phenotype is significantly enhanced by one copy of Df(2R)vg135, Df(2R)stil-A or Df(2R)stil-B, but is not significantly enhanced by one copy of stil1, stil4 or stil5. The dominant enhancement of the ovoD2 phenotype by Df(2R)vg135 is partially suppressed by a transgene carrying stil+. This suggests that the strong interaction between Df(2R)vg135 and ovoD2 is due to the deletion of two genes, one of which is stil.
In heterozygous females oogenesis is arrested. In the presence of either P{ovo-lacZ.B} or P{ovoM-D1} fertility of heterozygous females is significantly improved, average number of eggs laid rises from 2 to 30 and 24, respectively. For P{ovo-lacZ.B} up to 10% of eggs laid develop to adults, for P{ovoM-D1} only a small fraction of eggs develop. P{ovoM373} does not detectably change the ovoD2 phenotype.
Heterozygous females lay only very few eggs. Introduction of ovoB.T:Ecol\lacZ significantly increases the number of eggs laid. Laid eggs do not show any signs of development.
Most egg chambers of ovoD2/+ heterozygous ovaries arrest around oogenic stage 6 and very few vitellogenic oocytes are found. Two types of abnormal egg chambers occur. Pseudonurse cell chambers, where the egg chambers contain more than 15 nurse cells (though not usually more than 25) contain 0-2 oocyte nuclei. The second type of egg chamber contains largely undifferentiated germ cells, of indeterminate sex.
Phenotypic category: svb+.
Oogenesis in heterozygous females is mainly arrested prior to stage 6.
Permeable eggs.
Heterozygous females are fully sterile.
Most egg chambers arrest before vitellogenesis. Fertility is restored by the presence of two copies of ovo+.
Most of the egg chambers of heterozygous females fail to initiate vitellogenesis. The more advanced egg chambers often show a variety of abnormalities, such as permeability, flaccidity, absence of the anterior end of the chorion, fused dorsal appendages, egg chambers with more than 16 nuclei and occasionally, small ovarian tumours. Less than 30% of the wild-type number of eggs are laid per day. The soma is wild-type. Transheterozygotes with either ovoM1, ovoM2 or ovoD1rv20 have germ cells resembling early spermatocytes.
Mutant gene activity works in opposition to wild type activity. Viable. Male germ line is fertile, female germ line has permeable eggs.
Heterozygous females are completely sterile, producing only a few eggs throughout their lifetime, all of which fail to develop.
ovoD2 has female sterile | dominant phenotype, suppressible by Mmus\Ovol2A.hs
ovoD2 has female sterile | dominant phenotype, suppressible by ovo::Bole\ovoODP
ovoD2 has female sterile | dominant phenotype, suppressible by ovo::Bole\ovoODM
ovoD2 has decreased fecundity | dominant | female phenotype, suppressible by SxlfLS
ovoD2 has decreased fecundity | dominant | female phenotype, suppressible by SxlM1
ovoD2 has decreased fecundity | dominant | female phenotype, suppressible by Sxlf7,M1
ovoD2 has decreased fecundity | dominant | female phenotype, suppressible by SxlfP7B0
ovoD2 has decreased fecundity | dominant | female phenotype, suppressible by SxlfP7C2
ovoD2 has decreased fecundity | dominant | female phenotype, non-suppressible by SxlfPb
ovoD2 has decreased fecundity | dominant | female phenotype, non-suppressible by Sxlf9
ovoD2 has decreased fecundity | dominant | female phenotype, non-suppressible by Sxlf2
ovoD2 has decreased fecundity | dominant | female phenotype, non-suppressible by Sxlf18
The fraction of ovoD2/+ females that produce eggs is increased if the females express Mmus\Zfp339A.hs using a 1 hour heat shock at 37oC; 16-68% of the heat shocked females produce eggs, compared to 4% of control ovoD2/+ females. However, almost all the eggs laid by the ovoD2/+ females carrying Mmus\Zfp339A.hs fail to hatch.
The dominant female sterility of ovoD2 can be fully or partially rescued by ovo::Bole\ovoODM or ovo::Bole\ovoODP, depending on the transgenic line used.
One copy of P{ovo.S-7.2} fully rescues the sterility of heterozygous females.
Komitopoulou.
Clonal analysis shows that the dominant female sterile effect of ovoD2 is germ line autonomous.
Sxl alleles that have no known effect on the soma do not suppress the ovoD2 phenotype.
Intermediate ovo phenotype.
Partially suppresses the female-specific gonadal dysgenesis caused by hybrid dysgenesis at 27.5oC.
Shows a dominant interaction with otu alleles: more extreme mutant phenotype as assayed by reduction in number of egg chambers at stage 10 or further developed.