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Mechanistic basis of infertility of mouse intersubspecific hybrids

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    0397570 - ÚMG 2014 RIV US eng J - Článek v odborném periodiku
    Bhattacharyya, Tanmoy - Gregorová, Soňa - Mihola, Ondřej - Anger, Martin - Šebestová, J. - Denny, P. - Šimeček, Petr - Forejt, Jiří
    Mechanistic basis of infertility of mouse intersubspecific hybrids.
    Proceedings of the National Academy of Sciences of the United States of America. Roč. 110, č. 6 (2013), E468-E477. ISSN 0027-8424
    Grant CEP: GA MŠk(CZ) LD11079; GA MŠk(CZ) 1M0520; GA MŠk ED1.1.00/02.0109; GA ČR(CZ) GPP305/11/P630; GA ČR GA523/09/0743
    Grant ostatní: AV ČR(CZ) Premium Academiae of the Academy of Sciences of the Czech Republic; GA MŠk(CZ) ED1.1.00/02.0068
    Program: Akademická prémie - Praemium Academiae; ED
    Výzkumný záměr: CEZ:AV0Z50520514
    Institucionální podpora: RVO:68378050 ; RVO:67985904
    Klíčová slova: meiosis * meiotic sex chromosome inactivation * Prdm9 * chromosome substitution strains * Haldane's rule
    Kód oboru RIV: EB - Genetika a molekulární biologie
    Impakt faktor: 9.809, rok: 2013
    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3568299/

    According to the Dobzhansky-Muller model, hybrid sterility is a consequence of the independent evolution of related taxa resulting in incompatible genomic interactions of their hybrids. The model implies that the incompatibilities evolve randomly, unless a particular gene or nongenic sequence diverges much faster than the rest of the genome. Here we propose that asynapsis of heterospecific chromosomes in meiotic prophase provides a recurrently evolving trigger for the meiotic arrest of interspecific F1 hybrids. We observed extensive asynapsis of chromosomes and disturbance of the sex body in >95% of pachynemas of Mus m. musculus x Mus m. domesticus sterile F1 males. Asynapsis was not preceded by a failure of double-strand break induction, and the rate of meiotic crossing over was not affected in synapsed chromosomes. DNA double-strand break repair was delayed or failed in unsynapsed autosomes, and misexpression of chromosome X and chromosome Y genes was detected in single pachynemas and by genome-wide expression profiling. Oocytes of F1 hybrid females showed the same kind of synaptic problems but with the incidence reduced to half. Most of the oocytes with pachytene asynapsis were eliminated before birth. We propose the heterospecific pairing of homologous chromosomes as a preexisting condition of asynapsis in interspecific hybrids. The asynapsis may represent a universal mechanistic basis of F1 hybrid sterility manifested by pachytene arrest. It is tempting to speculate that a fast-evolving subset of the noncoding genomic sequence important for chromosome pairing and synapsis may be the culprit.
    Trvalý link: http://hdl.handle.net/11104/0227589

     
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