Onset and Progress of Meiotic Prophase in the Oocytes in the B6.YTIR Sex-Reversed Mouse Ovary1

Abstract

When the Y chromosome of a Mus musculus domesticus male mouse (caught in Tirano, Italy) is placed on a C57BL/6J genetic background, approximately half of the XY (B6.YTIR) progeny develop into normal-appearing but infertile females. We have previously reported that the primary cause of infertility can be attributed to their oocytes. To identify the primary defect in the XY oocyte, we examined the onset and progress of meiotic prophase in the B6.YTIR fetal ovary. Using bromo-deoxyuridine incorporation and culture, we determined that the germ cells began to enter meiosis at the developmental ages and in numbers comparable to those in the control XX ovary. Furthermore, the meiotic prophase appeared to progress normally until the late zygotene stage. However, the oocytes that entered meiosis early in the XY ovary failed to complete the meiotic prophase. On the other hand, a considerable number of oocytes entered meiosis at late developmental stages and completed the meiotic prophase in the XY ovary. We propose that the timing of entry into meiosis and the XY chromosomal composition influence the survival of oocytes during meiotic prophase in the fetal ovary.

The expression of Y-linked Zfy2 in XY mouse oocytes leads to frequent meiosis 2 defects, a high incidence of subsequent early cleavage stage arrest and infertility

“…Furthermore, oocyte deficiency has been reported in both XY Sry- and C57BL/6 XY females (Lovell-Badge and Robertson, 1990; Park and Taketo, 2003). Although oocyte count data are not available for XOs with a maternal X (X m O), in XY Sry- and XY d females the X usually fails to synapse with the Y, and, as in XOs, may be asynapsed or self-synapsed (Mahadevaiah et al, 1993) (our unpublished observations on XY d-1 ).…”

“…Based on previous observations suggesting substantial oocyte deficiency in XY Sry- and C57BL/6 XY females (Lovell-Badge and Robertson, 1990; Park and Taketo, 2003), our initial focus was on the possibility that XY Sry- females might have increased depletion of the oocyte pool in the perinatal period, but this proved not to be the case. Importantly, because the oocyte count data were obtained using the same quantitation technique used previously for X p O females (Burgoyne and Baker, 1985), these data show that a single maternal or paternal X is associated with substantial oocyte deficiency at this age.…”

Apoptosis in mouse fetal and neonatal oocytes during meiotic prophase one

“…The data were then analysed according to stage of meiotic prophase I on certain dpc, to determine whether oocytes entering meiosis earlier or later than average were more prone to apoptosis, as has been suggested by Park and Taketo [23]. …”

Retinoic acid, meiosis and germ cell fate in mammals

“…Therefore, the initial sex differentiation of a germ cell is determined not by its chromosomal constitution, but by its environment (McLaren, 1995;McLaren, 2003). However, the completion of meiosis and the formation of functional gametes are influenced by the sexchromosome composition of the germ cell (Amleh et al, 2000;Bradbury, 1983;Burgoyne, 1987;McLaren, 1981;Park and Taketo, 2003;Taketo-Hosotani et al, 1989).…”

“…Therefore, the initial sex differentiation of a germ cell is determined not by its chromosomal constitution, but by its environment (McLaren, 1995;McLaren, 2003). However, the completion of meiosis and the formation of functional gametes are influenced by the sexchromosome composition of the germ cell (Amleh et al, 2000;Bradbury, 1983;Burgoyne, 1987;McLaren, 1981;Park and Taketo, 2003;Taketo-Hosotani et al, 1989).A well-accepted hypothesis to explain the effect of tissue environment on germ cell fate has been that the developing testicular tissue produces a meiosis-inhibiting factor (Buehr et al, 1993;Francavilla and Zamboni, 1985;McLaren, 1984). This factor was supposedly produced at around 12.0 dpc by immature Sertoli cells, the supporting somatic cells in the developing testis, and considered likely to be a short-range diffusible factor (McLaren and Buehr, 1990;McLaren and Southee, 1997).…”