Mouse Molecular Genetics Group, Institute of Molecular Genetics, Academy of Sciences of the Czech Republic, 142 20 Prague, Czech Republic.
Proc Natl Acad Sci U S A. 2013 Feb 5;110(6):E468-77. doi: 10.1073/pnas.1219126110. Epub 2013 Jan 17.
According to the Dobzhansky-Muller model, hybrid sterility is a consequence of the independent evolution of related taxa resulting in incompatible genomic interactions of their hybrids. The model implies that the incompatibilities evolve randomly, unless a particular gene or nongenic sequence diverges much faster than the rest of the genome. Here we propose that asynapsis of heterospecific chromosomes in meiotic prophase provides a recurrently evolving trigger for the meiotic arrest of interspecific F1 hybrids. We observed extensive asynapsis of chromosomes and disturbance of the sex body in >95% of pachynemas of Mus m. musculus × Mus m. domesticus sterile F1 males. Asynapsis was not preceded by a failure of double-strand break induction, and the rate of meiotic crossing over was not affected in synapsed chromosomes. DNA double-strand break repair was delayed or failed in unsynapsed autosomes, and misexpression of chromosome X and chromosome Y genes was detected in single pachynemas and by genome-wide expression profiling. Oocytes of F1 hybrid females showed the same kind of synaptic problems but with the incidence reduced to half. Most of the oocytes with pachytene asynapsis were eliminated before birth. We propose the heterospecific pairing of homologous chromosomes as a preexisting condition of asynapsis in interspecific hybrids. The asynapsis may represent a universal mechanistic basis of F1 hybrid sterility manifested by pachytene arrest. It is tempting to speculate that a fast-evolving subset of the noncoding genomic sequence important for chromosome pairing and synapsis may be the culprit.
根据多布赞斯基-穆勒模型，杂种不育是相关分类单元独立进化的结果，导致它们的杂种之间基因组相互作用不相容。该模型意味着不相容性是随机进化的，除非特定基因或非基因序列的进化速度明显快于基因组的其他部分。在这里，我们提出，在减数分裂前期的异源染色体的不同步可能为种间 F1 杂种减数分裂的停滞提供了一个反复进化的触发因素。我们观察到>95%的 Mus m. musculus × Mus m. domesticus 不育 F1 雄性的 pachynemas 中广泛存在染色体不同步和性体紊乱。不同步并没有导致双链断裂诱导失败，而且联会染色体的减数交叉互换率不受影响。未联会的常染色体上的 DNA 双链断裂修复被延迟或失败，并且在单个 pachynemas 和全基因组表达谱中检测到染色体 X 和染色体 Y 基因的错误表达。F1 杂种雌性的卵母细胞也表现出同样的突触问题，但发生率降低到一半。大多数具有粗线期不同步的卵母细胞在出生前被淘汰。我们提出同源染色体的异源配对是种间杂种不同步的一个预先存在的条件。不同步可能代表了 F1 杂种不育的普遍机制基础，表现为粗线期停滞。人们不禁要推测，对于染色体配对和联会很重要的非编码基因组序列的一个快速进化子集可能是罪魁祸首。
