A single mutation results in diploid gamete formation and parthenogenesis in a Drosophila yemanuclein-alpha meiosis I defective mutant
1 Institut de Génétique Humaine (IGH), Unité Propre de Recherche 1142, Centre National de la Recherche Scientifique (CNRS), 141 Rue de la Cardonille, 34396 Montpellier cedex 5, France
2 Previous address: IBDML, Campus de Luminy Case 907, 13288 Marseille, Cedex 09, France
3 Previous address: Department of Biological Sciences, Stanford University, Stanford, CA94305, USA
4 Current Address: Cell Cycle and Cancer Biology Oklahoma Medical Research Foundation 825 N.E. 13th Street Oklahoma City, Oklahoma 73104 USA
BMC Genetics 2010, 11:104 doi:10.1186/1471-2156-11-104Published: 16 November 2010
Sexual reproduction relies on two key events: formation of cells with a haploid genome (the gametes) and restoration of diploidy after fertilization. Therefore the underlying mechanisms must have been evolutionary linked and there is a need for evidence that could support such a model.
We describe the identification and the characterization of yem1, the first yem-alpha mutant allele (V478E), which to some extent affects diploidy reduction and its restoration. Yem-alpha is a member of the Ubinuclein/HPC2 family of proteins that have recently been implicated in playing roles in chromatin remodeling in concert with HIRA histone chaperone. The yem1 mutant females exhibited disrupted chromosome behavior in the first meiotic division and produced very low numbers of viable progeny. Unexpectedly these progeny did not display paternal chromosome markers, suggesting that they developed from diploid gametes that underwent gynogenesis, a form of parthenogenesis that requires fertilization.
We focus here on the analysis of the meiotic defects exhibited by yem1 oocytes that could account for the formation of diploid gametes. Our results suggest that yem1 affects chromosome segregation presumably by affecting kinetochores function in the first meiotic division.
This work paves the way to further investigations on the evolution of the mechanisms that support sexual reproduction.