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Mechanisms of Transmission Ratio Distortion at Hybrid Sterility Loci Within and Between Mimulus Species

机译:杂种间和种间杂种不育位点的传递比畸变机理

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摘要

Hybrid incompatibilities are a common correlate of genomic divergence and a potentially important contributor to reproductive isolation. However, we do not yet have a detailed understanding of how hybrid incompatibility loci function and evolve within their native species, or why they are dysfunctional in hybrids. Here, we explore these issues for a well-studied, two-locus hybrid incompatibility between hybrid male sterility 1 (hms1) and hybrid male sterility 2 (hms2) in the closely related yellow monkeyflower species Mimulus guttatus and M. nasutus. By performing reciprocal backcrosses with introgression lines (ILs), we find evidence for gametic expression of the hms1-hms2 incompatibility. Surprisingly, however, hybrid transmission ratios at hms1 do not reflect this incompatibility, suggesting that additional mechanisms counteract the effects of gametic sterility. Indeed, our backcross experiment shows hybrid transmission bias toward M. guttatus through both pollen and ovules, an effect that is particularly strong when hms2 is homozygous for M. nasutus alleles. In contrast, we find little evidence for hms1 transmission bias in crosses within M. guttatus, providing no indication of selfish evolution at this locus. Although we do not yet have sufficient genetic resolution to determine if hybrid sterility and transmission ratio distortion (TRD) map to the same loci, our preliminary fine-mapping uncovers a genetically independent hybrid lethality system involving at least two loci linked to hms1. This fine-scale dissection of TRD at hms1 and hms2 provides insight into genomic differentiation between closely related Mimulus species and reveals multiple mechanisms of hybrid dysfunction.
机译:杂种不相容性是基因组差异的常见关联,并且可能是生殖分离的重要因素。但是,我们尚不了解杂种不兼容基因座如何在其天然物种中发挥功能和进化,或者为什么它们在杂种中功能失调。在这里,我们探索这些问题,以研究在密切相关的黄色猴种Miguus guttatus和M. nasutus中杂种雄性不育1(hms1)和杂种雄性不育2(hms2)之间的经过精心研究的两基因座杂种不相容性。通过执行与基因渗入系(IL)的对等回交,我们发现hms1-hms2不兼容的配子表达的证据。然而,令人惊讶的是,hms1处的杂种传播比率并未反映出这种不相容性,表明其他机制抵消了配子不育的影响。确实,我们的回交实验显示了通过花粉和胚珠向牙垢支原体的杂种传播偏向,当hms2对纳豆支原体等位基因纯合时,这种效应尤其明显。相比之下,我们几乎没有证据证明guttatus内杂交的hms1传播有偏差,没有提供此基因座自私进化的迹象。尽管我们还没有足够的遗传分辨率来确定杂种不育和传播比畸变(TRD)是否映射到同一基因座,但我们的初步精细映射揭示了一个遗传上独立的杂种致死系统,该系统涉及至少两个与hms1相关的基因座。在hms1和hms2处对TRD进行了精细的解剖,从而洞察了密切相关的 Mimulus 物种之间的基因组分化,并揭示了混合功能障碍的多种机制。

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