Wu Guangming, Hao Lanping, Han Zhiming, Gao Shaorong, Latham Keith E, de Villena Fernando Pardo-Manuel, Sapienza Carmen
Fels Institute for Cancer Research and Molecular Biology, Temple University School of Medicine, Philadelphia, Pennsylvania 19140, USA.
Genetics. 2005 May;170(1):327-34. doi: 10.1534/genetics.104.039479. Epub 2005 Mar 2.
We have observed maternal transmission ratio distortion (TRD) in favor of DDK alleles at the Ovum mutant (Om) locus on mouse chromosome 11 among the offspring of (C57BL/6 x DDK) F(1) females and C57BL/6 males. Although significant lethality occurs in this backcross ( approximately 50%), differences in the level of TRD found in recombinant vs. nonrecombinant chromosomes among offspring argue that TRD is due to nonrandom segregation of chromatids at the second meiotic division, i.e., true meiotic drive. We tested this hypothesis directly, by determining the centromere and Om genotypes of individual chromatids in zygote stage embryos. We found similar levels of TRD in favor of DDK alleles at Om in the female pronucleus and TRD in favor of C57BL/6 alleles at Om in the second polar body. In those embryos for which complete dyads have been reconstructed, TRD was present only in those inheriting heteromorphic dyads. These results demonstrate that meiotic drive occurs at MII and that preferential death of one genotypic class of embryo does not play a large role in the TRD.
我们在(C57BL/6×DDK)F(1)雌性与C57BL/6雄性杂交后代中,观察到小鼠11号染色体上卵母细胞突变体(Om)位点存在偏向DDK等位基因的母本传递比率畸变(TRD)。尽管在此回交中出现了显著的致死率(约50%),但后代中重组染色体与非重组染色体上TRD水平的差异表明,TRD是由于第二次减数分裂时染色单体的非随机分离,即真正的减数分裂驱动。我们通过确定合子期胚胎中单个染色单体的着丝粒和Om基因型,直接检验了这一假设。我们发现在雌原核中,Om位点存在偏向DDK等位基因的类似TRD水平,而在第二极体中,Om位点存在偏向C57BL/6等位基因的TRD。在那些已重建完整二分体的胚胎中,TRD仅存在于继承异型二分体的胚胎中。这些结果表明,减数分裂驱动发生在减数第二次分裂(MII),并且某一基因型胚胎的优先死亡在TRD中不起主要作用。