Verspoor Rudi L, Smith Jack M L, Mannion Natasha L M, Hurst Gregory D D, Price Tom A R
Institute of Integrative Biology University of Liverpool Liverpool L69 7ZB United Kingdom.
Evol Lett. 2018 May 10;2(3):169-179. doi: 10.1002/evl3.55. eCollection 2018 Jun.
Meiotically driving sex chromosomes manipulate gametogenesis to increase their transmission at a cost to the rest of the genome. The intragenomic conflicts they produce have major impacts on the ecology and evolution of their host species. However, their ecological dynamics remain poorly understood. Simple population genetic models predict meiotic drivers will rapidly reach fixation in populations and spread across landscapes. In contrast, natural populations commonly show spatial variation in the frequency of drivers, with drive present in clines or mosaics across species ranges. For example, harbors a sex ratio distorting drive chromosome (SR) at 15-25% frequency in North Africa, present at less than 2% frequency in adjacent southern Spain, and absent in other European populations. Here, we investigate the forces preventing the spread of the driver northward. We show that SR has remained at a constant frequency in North Africa, and failed to spread in Spain. We find strong evidence that spread is impeded by genetic incompatibility between SR and Spanish autosomal backgrounds. When we cross SR from North Africa onto Spanish genetic backgrounds we observe strong incompatibilities specific to hybrids bearing SR. The incompatibilities increase in severity in F2 male hybrids, leading to almost complete infertility. We find no evidence supporting an alternative hypothesis, that there is resistance to drive in Spanish populations. We conclude that the source of the stepped frequency variation is genetic incompatibility between the SR chromosome and the genetic backgrounds of the adjacent population, preventing SR spreading northward. The low frequency of SR in South Spain is consistent with recurrent gene flow across the Strait of Gibraltar combined with selection against the SR element through genetic incompatibility. This demonstrates that incompatibilities between drive chromosomes and naïve populations can prevent the spread of drive between populations, at a continental scale.
减数分裂驱动的性染色体操纵配子发生，以增加其传递频率，但这是以牺牲基因组的其他部分为代价的。它们所产生的基因组内冲突对其宿主物种的生态和进化具有重大影响。然而，它们的生态动态仍知之甚少。简单的群体遗传模型预测，减数分裂驱动因子将在种群中迅速固定并在整个区域传播。相比之下，自然种群中驱动因子的频率通常呈现空间变化，在物种分布范围内以渐变群或镶嵌形式存在。例如，在北非，一种性别比例扭曲的驱动染色体（SR）的频率为15%-25%，在相邻的西班牙南部频率低于2%，而在其他欧洲种群中则不存在。在这里，我们研究了阻止该驱动因子向北扩散的因素。我们发现，SR在北非一直保持着恒定的频率，并且未能在西班牙扩散。我们发现有力证据表明，SR与西班牙常染色体背景之间的遗传不兼容性阻碍了其扩散。当我们将来自北非的SR与西班牙遗传背景杂交时，我们观察到携带SR的杂种存在强烈的特异性不兼容性。在F2雄性杂种中，这些不兼容性的严重程度增加，导致几乎完全不育。我们没有找到支持另一种假设的证据，即西班牙种群对驱动有抗性。我们得出结论，频率阶梯变化的原因是SR染色体与相邻种群的遗传背景之间的遗传不兼容性，这阻止了SR向北扩散。西班牙南部SR的低频率与直布罗陀海峡的反复基因流动以及通过遗传不兼容性对SR元件的选择相一致。这表明，在大陆尺度上，驱动染色体与原始种群之间的不兼容性可以阻止驱动在种群之间的传播。
