Civetta Alberto
Department of Biology, University of Winnipeg, 515 Portage Ave., Winnipeg, MB, R3B 2E9, Canada.
J Mol Evol. 2016 May;82(4-5):176-82. doi: 10.1007/s00239-016-9734-z. Epub 2016 Mar 29.
Understanding the origin of species is of interest to biologist in general and evolutionary biologist in particular. Hybrid male sterility (HMS) has been a focus in studies of speciation because sterility imposes a barrier to free gene flow between organisms, thus effectively isolating them as distinct species. In this review, I focus on the role of differential gene expression in HMS and speciation. Microarray and qPCR assays have established associations between misregulation of gene expression and sterility in hybrids between closely related species. These studies originally proposed disrupted expression of spermatogenesis genes as a causative of sterility. Alternatively, rapid genetic divergence of regulatory elements, particularly as they relate to the male sex (fast-male evolution), can drive the misregulation of sperm developmental genes in the absence of sterility. The use of fertile hybrids (both backcross and F1 progeny) as controls has lent support to this alternative explanation. Differences in gene expression between fertile and sterile hybrids can also be influenced by a pattern of faster evolution of the sex chromosome (fast-X evolution) than autosomes. In particular, it would be desirable to establish whether known X-chromosome sterility factors can act as trans-regulatory drivers of genome-wide patterns of misregulation. Genome-wide expression studies coupled with assays of proxies of sterility in F1 and BC progeny have identified candidate HMS genes but functional assays, and a better phenotypic characterization of sterility phenotypes, are needed to rigorously test how these genes might contribute to HMS.
一般而言，生物学家，尤其是进化生物学家，都对物种起源感兴趣。杂种雄性不育一直是物种形成研究的重点，因为不育对生物体之间的自由基因流动构成了障碍，从而有效地将它们隔离为不同的物种。在这篇综述中，我将重点关注差异基因表达在杂种雄性不育和物种形成中的作用。微阵列和定量聚合酶链反应分析已经确定了基因表达失调与近缘物种杂种不育之间的关联。这些研究最初提出精子发生基因的表达中断是不育的原因。另外，调控元件的快速遗传分化，特别是与雄性相关的调控元件（快速雄性进化），在没有不育的情况下也可能导致精子发育基因的表达失调。使用可育杂种（回交和F1后代）作为对照为这一解释提供了支持。可育和不育杂种之间的基因表达差异也可能受到性染色体比常染色体更快进化模式（快速X进化）的影响。特别是，需要确定已知的X染色体不育因子是否可以作为全基因组表达失调模式的反式调控驱动因子。全基因组表达研究以及对F1和BC后代不育指标的分析已经确定了杂种雄性不育的候选基因，但需要进行功能分析以及对不育表型进行更好的表型特征描述，以便严格测试这些基因如何导致杂种雄性不育。
