The Jackson Laboratory, Bar Harbor, ME 04609, USA.
Department of Biology, Williams College, Williamstown, MA 01267, USA.
Genetics. 2021 Nov 5;219(3). doi: 10.1093/genetics/iyab136.
In species with single-locus, chromosome-based mechanisms of sex determination, the laws of segregation predict an equal ratio of females to males at birth. Here, we show that departures from this Mendelian expectation are commonplace in the 8-way recombinant inbred Collaborative Cross (CC) mouse population. More than one-third of CC strains exhibit significant sex ratio distortion (SRD) at wean, with twice as many male-biased than female-biased strains. We show that these pervasive sex biases persist across multiple breeding environments, are stable over time, and are not mediated by random maternal effects. SRD exhibits a heritable component, but QTL mapping analyses fail to nominate any large effect loci. These findings, combined with the reported absence of sex ratio biases in the CC founder strains, suggest that SRD manifests from multilocus combinations of alleles only uncovered in recombined CC genomes. We explore several potential complex genetic mechanisms for SRD, including allelic interactions leading to sex-biased lethality, genetic sex reversal, chromosome drive mediated by sex-linked selfish elements, and incompatibilities between specific maternal and paternal genotypes. We show that no one mechanism offers a singular explanation for this population-wide SRD. Instead, our data present preliminary evidence for the action of distinct mechanisms of SRD at play in different strains. Taken together, our work exposes the pervasiveness of SRD in the CC population and nominates the CC as a powerful resource for investigating diverse genetic causes of biased sex chromosome transmission.
在具有单基因座、基于染色体的性别决定机制的物种中,分离定律预测出生时雌性和雄性的比例相等。在这里,我们表明,在 8 种重组近交系协作交叉 (CC) 小鼠群体中,这种孟德尔预期的偏离是很常见的。超过三分之一的 CC 品系在断奶时表现出明显的性别比例失调 (SRD),雄性偏倚的品系是雌性偏倚的两倍多。我们表明,这些普遍存在的性别偏差在多个繁殖环境中持续存在,随着时间的推移保持稳定,并且不受随机母性效应的影响。SRD 具有遗传成分,但 QTL 映射分析未能确定任何大的效应基因座。这些发现,加上 CC 创始品系中报告的性别比例偏差不存在,表明 SRD 仅在重组 CC 基因组中揭示的等位基因的多基因座组合中表现出来。我们探讨了几种潜在的复杂遗传机制,包括导致性别偏倚致死的等位基因相互作用、遗传性别反转、由性连锁自私元件介导的染色体驱动以及特定母本和父本基因型之间的不兼容。我们表明,没有一种机制可以单一解释这种全种群的 SRD。相反,我们的数据初步证明了不同机制在不同品系中发挥作用的性别比例失调。总之,我们的工作揭示了 CC 群体中 SRD 的普遍性,并提名 CC 作为研究偏性性染色体传递的不同遗传原因的强大资源。