Abstract
Sexual reproduction is essential for many organisms to propagate themselves. It requires the formation of haploid female and male gametes: oocytes and sperms. These specialized cells are generated through meiosis, a particular type of cell division that produces cells with recombined genomes that differ from their parental origin. In this review, we highlight the end process of female meiosis, the divisions per se, and how they can give rise to a functional female gamete preparing itself for the ensuing zygotic development. In particular, we discuss why such an essential process in the propagation of species is so poorly controlled, producing a strong percentage of abnormal female gametes in the end. Eventually, we examine aspects related to the lack of centrosomes in female oocytes, the asymmetry in size of the mammalian oocyte upon division, and in mammals the direct consequences of these long-lived cells in the ovary.
Highlights
Sexual reproduction is essential for many organisms to propagate themselves
Amazing progress has been made since the pioneering review that put into the limelight the fact that human oocytes are error prone and that the rate of errors increases with the age of the mother[1]
Advance has come from studies on diverse model systems presenting both similarities and differences with human oocyte meiosis
Summary
Amazing progress has been made since the pioneering review that put into the limelight the fact that human oocytes are error prone and that the rate of errors increases with the age of the mother[1]. Advance has come from studies on diverse model systems presenting both similarities and differences with human oocyte meiosis. Observations made in human oocytes have been challenged by hypotheses tested in model systems where genetics or biochemistry can be performed. Many other factors not highlighted here, such as the distribution as well as the rate of recombination between homologues, which have a direct influence on chromosome segregation, can predispose for aneuploidy in oocytes[3]. The major discovery of PRDM9, a key factor controlling the distribution of hot spots for recombination in some species but not others, will certainly help us to understand the impact of recombination on aneuploidy in oocytes[94,95,96]. Grant information The author(s) declared that no grants were involved in supporting this work
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