Pardo-Manuel de Villena F, de la Casa-Esperon E, Briscoe T L, Sapienza C
Fels Institute for Cancer Research and Molecular Biology, Temple University School of Medicine, Philadelphia, Pennsylvania 19140, USA.
Genetics. 2000 Jan;154(1):333-42. doi: 10.1093/genetics/154.1.333.
We have shown previously that the progeny of crosses between heterozygous females and C57BL/6 males show transmission ratio distortion at the Om locus on mouse chromosome 11. This result has been replicated in several independent experiments. Here we show that the distortion maps to a single locus on chromosome 11, closely linked to Om, and that gene conversion is not implicated in the origin of this phenomenon. To further investigate the origin of the transmission ratio distortion we generated a test using the well-known effect of recombination on maternal meiotic drive. The genetic test presented here discriminates between unequal segregation of alleles during meiosis and lethality, based on the analysis of genotype at both the distorted locus and the centromere of the same chromosome. We used this test to determine the cause of the transmission ratio distortion observed at the Om locus. Our results indicate that transmission ratio distortion at Om is due to unequal segregation of alleles to the polar body at the second meiotic division. Because the presence of segregation distortion at Om also depends on the genotype of the sire, our results confirm that the sperm can influence segregation of maternal chromosomes to the second polar body.
我们之前已经表明,杂合雌性与C57BL/6雄性杂交的后代在小鼠11号染色体上的Om位点表现出传递比率畸变。这一结果已在多个独立实验中得到重复。在此我们表明,这种畸变定位于11号染色体上的一个单一基因座,与Om紧密连锁,并且基因转换与这一现象的起源无关。为了进一步研究传递比率畸变的起源,我们利用重组对母本减数分裂驱动的已知效应进行了一项测试。这里呈现的基因测试基于对同一染色体上畸变基因座和着丝粒处基因型的分析,区分减数分裂过程中等位基因的不等分离和致死性。我们使用这个测试来确定在Om位点观察到的传递比率畸变的原因。我们的结果表明,Om位点的传递比率畸变是由于在第二次减数分裂时等位基因向极体的不等分离。由于Om位点分离畸变的存在也取决于父本的基因型,我们的结果证实精子可以影响母本染色体向第二极体的分离。