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Published 22 May 2006. doi:10.1083/jcb.200512077
The Rockefeller University Press, 0021-9525 $8.00
JCB, Volume 173, Number 4, 485-495
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Article

 Structural damage to meiotic chromosomes impairs DNA recombination and checkpoint control in mammalian oocytes

Hong Wang and Christer Höög

Department of Cell and Molecular Biology, Karolinska Institutet, SE-171 77 Stockholm, Sweden

Correspondence to Christer Höög: christer.hoog{at}ki.se

Meiosis in human oocytes is a highly error-prone process with profound effects on germ cell and embryo development. The synaptonemal complex protein 3 (SYCP3) transiently supports the structural organization of the meiotic chromosome axis. Offspring derived from murine Sycp3–/– females die in utero as a result of aneuploidy. We studied the nature of the proximal chromosomal defects that give rise to aneuploidy in Sycp3–/– oocytes and how these errors evade meiotic quality control mechanisms. We show that DNA double-stranded breaks are inefficiently repaired in Sycp3–/– oocytes, thereby generating a temporal spectrum of recombination errors. This is indicated by a strong residual {gamma}H2AX labeling retained at late meiotic stages in mutant oocytes and an increased persistence of recombination-related proteins associated with meiotic chromosomes. Although a majority of the mutant oocytes are rapidly eliminated at early postnatal development, a subset with a small number of unfinished crossovers evades the DNA damage checkpoint, resulting in the formation of aneuploid gametes.

Abbreviations used in this paper: AE, axial element; dpp, days postpartum; DSB, double-stranded break; E, embryonic day; SC, synaptonemal complex; SYCP, synaptonemal complex protein.


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