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A single mutation results in diploid gamete formation and parthenogenesis in a Drosophila yemanuclein-alpha meiosis I defective mutant

BACKGROUND: 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. R...

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Detalles Bibliográficos
Autores principales: Meyer, Régis E, Delaage, Michèle, Rosset, Roland, Capri, Michèle, Aït-Ahmed, Ounissa
Formato: Texto
Lenguaje:English
Publicado: BioMed Central 2010
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2998452/
https://www.ncbi.nlm.nih.gov/pubmed/21080953
http://dx.doi.org/10.1186/1471-2156-11-104
Descripción
Sumario:BACKGROUND: 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. RESULTS: We describe the identification and the characterization of yem(1), 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 yem(1 )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. CONCLUSIONS: We focus here on the analysis of the meiotic defects exhibited by yem(1 )oocytes that could account for the formation of diploid gametes. Our results suggest that yem(1 )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.