svb, shavenbaby, shaven baby, ovoD, ovo/svb
Gene model reviewed during 5.43
Low-frequency RNA-Seq exon junction(s) not annotated.
Annotated transcripts do not represent all possible combinations of alternative exons and/or alternative promoters.
Gene model reviewed during 5.52
Only 3 of the 4 C2H2-type zinc-fingers are required for DNA-binding. Based on its marked lack of evolutionary conservation, the fourth zinc-finger is unlikely to be required.
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\ovo using the Feature Mapper tool.
GBrowse - Visual display of RNA-Seq signalsView Dmel\ovo in GBrowse 2
Please Note This section lists cDNAs and ESTs that fall within the genomic extent of the gene model, which may include cDNAs and ESTs of genes within introns, or of overlapping genes. Please see GBrowse for alignment of the cDNAs and ESTs to the gene model.
For each fully sequenced cDNA the DGRC maintains various forms of the cDNA (e.g tagged or untagged) in several different host vectors for subsequent cloning and expression in Drosophila and Drosophila cell lines.
Source for identity of: ovo CG6824
Source for merge of: ovo CG15467
Annotations CG6824 and CG15467 merged as CG6824 (which corresponds to ovo) in release 3 of the genome annotation.
Recessive alleles, mostly recovered as revertants of dominant alleles, usually but not always, simultaneously mutant lzl; The lzl eye phenotype is cold-sensitive and semidominant. Most revertants are amorphic in that, when tested in heterozygous combination with ovoD1rv22 or ovoD1rv23, they have atrophic ovaries, with no egg chambers observable.
Expression is enriched in embryonic gonads.
ovo is a key selector gene that, cell autonomously, directs cytoskeletal modifications producing the denticle.
Analysis of dominant-negative ovoD mutations suggests that the dominant activity is due to the new initiation codons in the ovo-B isoform mRNAs and not due to the amino acid substitutions in the ovo-A isoform.
High ovo+ copy number is not sufficient for overt development of XY germ cells. The absence of ovo+ in XX germ cells results in altered sex determination and cell viability, but increased ovo+ activity in XY germ cells is insufficient to impair germline viability and is probably insufficient to alter sexual identity.
The dominant-negative effects of the ovoD mutations are likely to arise from the expression of novel protein isoforms, starting during germline cell differentiation.
Female germ cells require zygotic ovo function for survival mainly during the second larval, third larval and pupal stages.
otu and ovo are required cell autonomously in the female germline for germ cell proliferation and differentiation. XY germ cells do not require otu when developing in testes, but become dependent on otu function for proliferation when placed in an ovary. The requirement for ovo is dependent on a cell autonomous signal derived from the X:A ratio. The differential regulation of the otu and ovo genes provides a mechanism for the female germline to incorporate both somatic and cell-autonomous inputs required for oogenesis.
300 deficiency chromosomes have been screened for enhancers and suppressors of the ovo mutant phenotype. More than a dozen small regions probably contain genes whose products act in developmental hierarchies that include ovo+ protein.
Zygotic ovo activity is not essential for pole cell viability or proliferation during stages of embryogenesis. Pupal gonads fail to produce egg chambers indicating that the agametic adult phenotype is caused by a block in oogenesis before cyst formation, rather than the degeneration of existing egg chambers. ovo function is not essential for germline viability before pupariation.
An insertion of a transgene containing the ovoD1 mutation onto an autosome can confer a dominant female sterile phenotype.
The genetic hierarchy regulating female germ-line sex determination includes tra, tra2, dsx, fu, otu, ovo, snf and Sxl. otu+, ovo+ and snf+ activities are required for female-specific Sxl+ pre-mRNA splicing within 2X germ-line cells.
Phenotypic analysis of mutations suggests that ovo encodes a function necessary for normal development of the oocyte.
ovo appears to be involved in germ line sex determination and is linked in some manner to sex determination in the soma.
Molecular analysis of ovo revertants from a cross with the y v f mal strain demonstrate they have acquired either a gypsy or copia insertion at cytological location 4E.
ovo is required for early female germ line maintenance but is not required for male germ line stability.
ovo mutants display short denticles that are reduced in number and an absence of dorsal hairs.
The expression of genes controlling neurogenesis is dependent on the previous activity of the genes controlling the development of the embryonic dorsal-ventral pattern.
All ovo alleles fully penetrant for female sterility; no male function for ovo+ known. Lack of zygotic activity results in complete absence of germ-line cells in adult female; reduction in numbers of germ cells first evident during early gastrulation. Homozygotes for weaker alleles produce germ cells, but oogenesis defective; egg chambers may degenerate prior to vitellogenesis or proceed through oogenesis and be oviposited, depending on allele; laid eggs are permeable to neutral red and never develop. Heterozygotes for two of the dominant alleles phenotypically similar to homozygotes for weak recessive alleles. Ovarian tumors formed in females carrying ovoD3 in heterozygous combination with the hypomorphic alleles, e.g., ovoD1rv20, or with snf. The ovoD2 mutation is partially suppressed by many Sxl alleles. ovoD1/+ females produce no eggs; extensively utilized in the selection of ovo+ germ-line clones. svb alleles are homozygous lethal. Many fewer denticles than wild type; remaining denticles small and with characteristic morphology. Denticles arranged in belts in the abdominal segments; absent from thoracic segments. Cell autonomous in mosaics; useful in studying embryonic mosaics.