title: Both nuclear and cytoplasmic components are defective in oocytes of the B6.Y(TIR) sex-reversed female mouse.
abstract: In the mammalian gonadal primordium, activation of the Sry gene on the Y chromosome initiates a cascade of genetic events leading to testicular organization whereas its absence results in ovarian differentiation. An exception occurs when the Y chromosome of Mus musculus domesticus from Tirano, Italy (Y(TIR)), is placed on the C57BL/6J (B6) genetic background. The B6.Y(TIR) progeny develop only ovaries or ovotestes despite Sry transcription in fetal life. Consequently, the XY offspring with bilateral ovaries develop into apparently normal females, but their eggs fail to develop after fertilization. Our previous studies have shown that the primary cause of infertility can be attributed to oocytes rather than their surrounding somatic cells in the XY ovary. This study attempted to identify the defects in oocytes from the B6.Y(TIR) female mouse. We examined the developmental potential of embryos from XY and XX females after exchanging their nuclear components by microsurgery following in vitro maturation and fertilization. The results suggest that both nuclear and cytoplasmic components are defective in oocytes from XY females. In the XY fetal ovary, most germ cells entered meiosis and their autosomes appeared to synapse normally while the X and Y chromosomes remained unpaired during meiotic prophase. This lack of X-Y pairing probably caused aneuploidy in some secondary oocytes following in vitro maturation. However, normal numbers of chromosomes in the rest of the secondary oocytes indicate that aneuploidy alone can not explain the nuclear defect in oocytes.
authors.affiliation: Urology Research Laboratory, Department of Surgery, McGill University, Montreal, Quebec, H3A 1A1, Canada.
authors.forename: A
authors.initials: A
authors.lastname: Amleh
authors.forename: L
authors.initials: L
authors.lastname: Smith
authors.forename: H
authors.initials: H
authors.lastname: Chen
authors.forename: T
authors.initials: T
authors.lastname: Taketo
mesh_terms: D000782:Aneuploidy; D000818:Animals; D002467:Cell Nucleus / Q000648:ultrastructure; D003593:Cytoplasm / Q000648:ultrastructure; D004268:DNA-Binding Proteins / Q000235:genetics*; D012734:Disorders of Sex Development; D004624:Embryo Transfer; D005260:Female; D008297:Male; D008540:Meiosis / Q000235:genetics; D051379:Mice; D008810:Mice, Inbred C57BL; D009687:Nuclear Proteins; D009865:Oocytes / Q000254:growth & development / Q000648:ultrastructure*; D019849:Sex Determination Processes; D051876:Sex-Determining Region Y Protein; D014157:Transcription Factors; D014960:X Chromosome / Q000235:genetics; D014998:Y Chromosome / Q000235:genetics*; D015053:Zygote / Q000648:ultrastructure
chemical_list: D004268:DNA-Binding Proteins; D009687:Nuclear Proteins; D051876:Sex-Determining Region Y Protein; C497746:Sry protein, mouse; D014157:Transcription Factors