Pardo-Manual de Villena F, Slamka C, Fonseca M, Naumova A K, Paquette J, Pannunzio P, Smith M, Verner A, Morgan K, Sapienza C
Fels Institute for Cancer Research, Temple University School of Medicine, Philadelphia, Pennsylvania 19140, USA.
Genetics. 1996 Apr;142(4):1299-304. doi: 10.1093/genetics/142.4.1299.
We determined the genotypes of > 200 offspring that are survivors of matings between female reciprocal F1 hybrids (between the DDK and C57BL/6J inbred mouse strains) and C57BL/6J males at markers linked to the Ovum mutant (Om) locus on chromosome 11. In contrast to the expectations of our previous genetic model to explain the "DDK syndrome, " the genotypes of these offspring do not reflect preferential survival of individuals that receive C57BL/6J alleles from the F1 females in the region of chromosome 11 to which the Om locus has been mapped. In fact, we observe significant transmission-ratio distortion in favor of DDK alleles in this region. These results are also in contrast to the expectations of Wakasugi's genetic model for the inheritance of Om, in which he proposed equal transmission of DDK and non-DDK alleles from F1 females. We propose that the results of these experiments may be explained by reduced expression of the maternal DDK Om allele or expression of the maternal DDK Om allele in only a portion of the ova of F1 females.
我们确定了200多个后代的基因型，这些后代是雌性相互杂交F1代（DDK和C57BL/6J近交系小鼠品系之间）与C57BL/6J雄性小鼠交配的幸存者，这些后代在与11号染色体上的卵子突变体（Om）位点连锁的标记处进行检测。与我们之前解释“DDK综合征”的遗传模型预期相反，这些后代的基因型并未反映出在11号染色体上Om位点所在区域从F1雌性那里获得C57BL/6J等位基因的个体的优先存活情况。事实上，我们观察到在该区域存在显著的偏向DDK等位基因的传递率扭曲现象。这些结果也与若杉关于Om遗传的遗传模型预期相反，在他的模型中，他提出F1雌性的DDK和非DDK等位基因会等量传递。我们认为，这些实验结果或许可以通过母本DDK Om等位基因表达降低，或者母本DDK Om等位基因仅在F1雌性的一部分卵子中表达来解释。
