Department of Biology, Hong Kong Baptist University, Hong Kong, China.
Department of Biology, Hong Kong Baptist University, Hong Kong, China
Genetics. 2019 Jul;212(3):801-813. doi: 10.1534/genetics.119.302202. Epub 2019 May 7.
Hybrid male progeny from interspecies crosses are more prone to sterility or inviability than hybrid female progeny, and the male sterility and inviability often demonstrate parent-of-origin asymmetry. However, the underlying genetic mechanism of asymmetric sterility or inviability remains elusive. We previously established a genome-wide hybrid incompatibility (HI) landscape between and by phenotyping a large collection of strains each carrying a introgression. In this study, we systematically dissect the genetic mechanism of asymmetric sterility and inviability in both hybrid male and female progeny between the two species. Specifically, we performed reciprocal crosses between and different strains that each carry a GFP-labeled genomic fragment referred to as introgression, and scored the HI phenotypes in the F1 progeny. The aggregated introgressions cover 94.6% of the genome, including 100% of the chromosome. Surprisingly, we observed that two fragments that produce male sterility as an introgression rescued hybrid F1 sterility in males fathered by Subsequent backcrossing analyses indicated that a specific interaction between the -linked interaction and one autosome introgression is required to rescue the hybrid male sterility. In addition, we identified another two genomic intervals on chromosomes II and IV that can rescue the inviability, but not the sterility, of hybrid F1 males fathered by , suggesting the involvement of differential epistatic interactions in the asymmetric hybrid male fertility and inviability. Importantly, backcrossing of the rescued sterile males with led to the isolation of a 1.1-Mb genomic interval that specifically interacts with an -linked introgression, which is essential for hybrid male fertility. We further identified three genomic intervals on chromosome I, II, and III that produced inviability in all F1 progeny, dependent on or independent of the parent-of-origin. Taken together, we identified multiple independent interacting loci that are responsible for asymmetric hybrid male and female sterility, and inviability, which lays a foundation for their molecular characterization.
种间杂交的雄性后代比雌性后代更容易不育或夭折，而且雄性不育和夭折通常表现出亲源性不对称。然而，不对称不育或夭折的潜在遗传机制仍难以捉摸。我们之前通过表型分析大量携带 渐渗片段的 菌株，建立了 和 之间的全基因组杂交不亲和（HI）景观。在这项研究中，我们系统地剖析了这两个物种之间杂交雄性和雌性后代不对称不育和夭折的遗传机制。具体来说，我们在 和不同的 菌株之间进行了正反杂交，这些菌株都携带一个 GFP 标记的 基因组片段，称为渐渗片段，并在 F1 后代中对 HI 表型进行了评分。聚合的渐渗片段涵盖了 94.6%的 基因组，包括 100%的 染色体。令人惊讶的是，我们观察到两个导致 雄性不育的 片段作为渐渗片段拯救了由 产生的杂交 F1 雄性不育。随后的回交分析表明，-连锁互作和一个常染色体渐渗片段之间的特定相互作用是拯救杂交雄性不育所必需的。此外，我们在染色体 II 和 IV 上确定了另外两个 基因组区间，它们可以拯救由 产生的不育杂交 F1 雄性的活力，但不能拯救其不育性，这表明在不对称杂交雄性育性和活力中涉及不同的上位性相互作用。重要的是，与 回交的被拯救的不育雄性与 杂交导致了一个 1.1-Mb 基因组区间的分离，该区间与 -连锁渐渗片段特异性相互作用，这对于杂交雄性育性是必需的。我们进一步鉴定了三个 基因组区间，分别位于染色体 I、II 和 III 上，这些区间在所有 F1 后代中都导致了活力丧失，这取决于或独立于亲源性。总之，我们确定了多个独立的相互作用位点，它们负责不对称杂交雄性和雌性不育和夭折，为它们的分子特征奠定了基础。
