Disease relevance of ovo

• We find that svb is a key selector gene that, cell autonomously, directs cytoskeletal modifications producing the denticle [1].
• Severe alleles of the ovarian tumor (otu) and ovo genes result in female sterility in Drosophila melanogaster, producing adult ovaries that completely lack egg chambers [2].
• The gypsy retrovirus invades the germ line of Drosophila females, inserting with a high frequency into the ovo locus [3].

High impact information on ovo

• Conversely, Wingless promotes the smooth cell fate through the transcriptional repression of svb by the bipartite nuclear factor Armadillo/dTcf [1].
• The DER pathway promotes denticle formation by activating svb expression [1].
• Ovo/svb is a complex gene with two genetic functions corresponding to separate control regions: ovo is required for female germline development and svb for epidermal morphogenesis [1].
• The ovo gene required for cuticle formation and oogenesis in flies is involved in hair formation and spermatogenesis in mice [4].
• Mutations at the ovo locus result in a defective female germ line [5].

Biological context of ovo

• We propose that 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 [6].
• Finally, we show that the gene dosage of otu modifies the phenotype of ovaries heterozygous for the dominant alleles of ovo, another gene involved in germ line sex determination [7].
• Drosophila OVO regulates ovarian tumor transcription by binding unusually near the transcription start site [8].
• Three OVO-binding sites exist in a compact regulatory region that controls germline expression of the otu gene [8].
• The ovo gene of Drosophila encodes a zinc finger protein required for female germ line development [9].

Anatomical context of ovo

• By using various ovo-lacZ reporter genes, we determined that the long Ovo isoforms starting at methionine M1, present in transcripts ovo alpha, are expressed at low levels only in mature oocytes [10].
• Our examination of ovo null mutant organelles demonstrate that it is required for the differentiation of XX germ cells during larval gonial stages, in addition to its known role in maintaining germ cell numbers [11].
• We have mapped the ovo locus to position 4E1-2 of the salivary gland X chromosome by using a set of cytologically visible deletions [5].
• Expression of murine novel zinc finger proteins highly homologous to Drosophila ovo gene product in testis [12].
• Essentially the same rules for siRNA sequence preference were found applicable to DNA-based RNAi in mammalian cells and in ovo RNAi using chick embryos [13].

Associations of ovo with chemical compounds

• We report here that all three ovoD mutations are point mutations that create new in-frame methionine codons in the 5' part of ovo [10].

Physical interactions of ovo

• Interestingly, the strongest OVO-binding site is very near the otu transcription start, where basal transcriptional complexes must function [8].

Regulatory relationships of ovo

• One of two loss-of-function ovo alleles is suppressed by a loss-of-function Sex-lethal allele [14].
• EGL-38 Pax regulates the ovo-related gene lin-48 during Caenorhabditis elegans organ development [15].

Other interactions of ovo

• Our data indicate that transcriptional regulation of svb integrates inputs from the Wingless and DER pathways and controls epidermal differentiation [1].
• If Serrate-Notch signaling is absent, the denticle field narrows while the smooth cell field expands, as judged by the expression of the denticle field determinant Ovo/Shaven baby [16].
• Using P[stil+] transgenes, we show that stil and a closely localized gene are involved in the modification of the ovarian phenotypes of the dominant alleles of ovo caused by heterozygosity of region 49 A-D [17].
• A loss-of-function allele of ovo is epistatic to germ line dependent mutations in Sex-lethal [14].
• Ectopic expression of lunatic Fringe leads to downregulation of Serrate-1 in the developing chick neural tube; analysis using in ovo electroporation transfection technique [18].

Analytical, diagnostic and therapeutic context of ovo

• In ovo electroporation on E2 chick brain with the eucaryotic expression vector that encodes chick Pax-5 cDNA was used [19].
• By using various genomic probes for in situ hybridization to wild type and mutant embryos, we show that ovo indeed shares most of its coding sequences with svb. svb expression is detected early in the presumptive head region and later in each segment [20].
• Genetic mapping experiments and interspecific complementation tests indicate that this difference is caused, in its entirety, by evolution at the ovo/shaven-baby locus [21].

References