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• W2065016097 abstract "For at least 5% of all clinically recognized human pregnancies, meiotic segregation errors give rise to zygotes with the wrong number of chromosomes [1Hassold T Hunt P To err (meiotically) is human the genesis of human aneuploidy.Nat. Rev. Genet. 2001; 2: 280-291Crossref PubMed Scopus (1618) Google Scholar]. Although most aneuploid fetuses perish in utero, trisomy in liveborns is the leading cause of mental retardation [2Hassold T Hunt P.A Sherman S Trisomy in humans incidence, origin and etiology.Curr. Opin. Genet. Dev. 1993; 3: 398-403Crossref PubMed Scopus (123) Google Scholar]. A large percentage of human trisomies originate from segregation errors during female meiosis I; such errors increase in frequency with maternal age [1Hassold T Hunt P To err (meiotically) is human the genesis of human aneuploidy.Nat. Rev. Genet. 2001; 2: 280-291Crossref PubMed Scopus (1618) Google Scholar]. Despite the clinical importance of age-dependent nondisjunction in humans, the underlying mechanisms remain largely unexplained. Efforts to recapitulate age-dependent nondisjunction in a mammalian experimental system have so far been unsuccessful. Here we provide evidence that Drosophila is an excellent model organism for investigating how oocyte aging contributes to meiotic nondisjunction. As in human oocytes, nonexchange homologs and bivalents with a single distal crossover in Drosophila oocytes are most susceptible to spontaneous nondisjunction during meiosis I [3Koehler K.E Boulton C.L Collins H.E French R.L Herman K.C Lacefield S.M Madden L.D Schuetz C.D Hawley R.S Spontaneous X chromosome MI and MII nondisjunction events in Drosophila melanogaster oocytes have different recombinational histories.Nat. Genet. 1996; 14: 406-413Crossref PubMed Scopus (119) Google Scholar, 4MacDonald M Hassold T Harvey J Wang L.H Morton N.E Jacobs P The origin of 47,XXY and 47,XXX aneuploidy heterogeneous mechanisms and role of aberrant recombination.Hum. Mol. Genet. 1994; 3: 1365-1371Crossref PubMed Scopus (143) Google Scholar, 5Lamb N Freeman S.B Savage-Austin A Pettay D Taft L Hersey J Gu Y Shen J Saker D May K.M et al.Susceptible chiasmate configurations of chromosome 21 predispose to non-disjunction in both maternal meiosis I and meiosis II.Nat. Genet. 1996; 14: 400-405Crossref PubMed Scopus (304) Google Scholar, 6Hassold T Merrill M Adkins K Freeman S Sherman S Recombination and maternal age-dependent nondisjunction molecular studies of trisomy 16.Am. J. Hum. Genet. 1995; 57: 867-874PubMed Google Scholar]. We show that in a sensitized genetic background in which sister chromatid cohesion is compromised, nonrecombinant X chromosomes become vulnerable to meiotic nondisjunction as Drosophila oocytes age. Our data indicate that the backup pathway that normally ensures proper segregation of achiasmate chromosomes deteriorates as Drosophila oocytes age and provide an intriguing paradigm for certain classes of age-dependent meiotic nondisjunction in humans." @default.
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• W2065016097 date "2003-03-01" @default.
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• W2065016097 title "A Model System for Increased Meiotic Nondisjunction in Older Oocytes" @default.
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• W2065016097 doi "https://doi.org/10.1016/s0960-9822(03)00134-9" @default.
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