Hybrid sterility with meiotic metaphase arrest in intersubspecific mouse crosses.
Hybrid sterility with meiotic metaphase arrest in intersubspecific mouse crosses.
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亚种间小鼠杂交中减数分裂中期停滞的杂种不育。
DOI：
10.1093/jhered/esy060
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发表时间：
2019
期刊：
影响因子：
--
通讯作者：
Fujiwara Y.
中科院分区：
文献类型：
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作者：
Nishino R;Petri S;Handel MA;Kunieda T;Fujiwara Y.
尽管属于不同物种和亚种的生物有时会产生可育的后代，但物种形成过程的一个标志是生殖隔离，其特征是由于配子发生失败而导致的杂种不育（HS）。在哺乳动物中，HS 通常由雄性（异配性别）表现出来。 HS的表型表现很复杂。最常见的是常染色体和性染色体相互作用的异常，这些异常与减数分裂前期停滞或减数分裂后精子发生畸变有关，并导致配子缺陷或缺失。本研究的目的是确定由 Mos musculus molossinus 衍生品系和不同 Mus musculus Domesticus 近交实验室小鼠品系交配产生的亚种间 F1 小鼠的 HS 表型。大多数这些杂交产生了可育的 F1 后代。然而，当雌性 BALB/cJ (domesticus) 小鼠与雄性 JF1/MsJ (molossinus) 小鼠交配时，(BALBdomxJF1mol)F1 雄性小鼠是不育的，而通过相互杂交产生的 (JF1molxBALBdom)F1 雄性小鼠是可育的；因此不育表型是不对称的。不育 (BALBdomxJF1mol) F1 雄性表现出高频率的减数分裂中期停滞和错位染色体，可能与高频率的 XY 解离有关。有趣的是，在不育 (BALBdomxJF1mol)F1 雄性中，我们观察到几个减数分裂基因的异常等位基因特异性表达，这些基因在包括染色体配对在内的重要减数分裂事件中发挥关键作用。总之，亚种间 F1 雄性中不对称 HS 表型的观察结果可能是由于 XY 染色体对减数分裂行为的减数分裂缺陷以及减数分裂基因的转录失调所致，为理解哺乳动物的物种形成机制提供了新的模型和方向。
Although organisms belonging to different species and subspecies sometimes produce fertile offspring, a hallmark of the speciation process is reproductive isolation, characterized by hybrid sterility (HS) due to failure in gametogenesis. In mammals, HS is usually exhibited by males, the heterogametic sex. The phenotypic manifestations of HS are complex. The most frequently observed are abnormalities in both autosomal and sex chromosome interactions that are linked to meiotic prophase arrest or postmeiotic spermiogenesis aberrations and lead to defective or absent gametes. The aim of this study was to determine the HS phenotypes in intersubspecific F1mice produced by matings betweenMus musculus molossinus-derived strains and diverseMus musculus domesticus-inbred laboratory mouse strains. Most of these crosses produced fertile F1offspring. However, when female BALB/cJ (domesticus) mice were mated to male JF1/MsJ (molossinus) mice, the (BALBdomxJF1mol)F1males were sterile, whereas the (JF1molxBALBdom)F1males produced by the reciprocal crossings were fertile; thus the sterility phenotype was asymmetric. The sterile (BALBdomxJF1mol) F1males exhibited a high rate of meiotic metaphase arrest with misaligned chromosomes, probably related to a high frequency of XY dissociation. Intriguingly, in the sterile (BALBdomxJF1mol)F1males we observed aberrant allele-specific expression of several meiotic genes, that play critical roles in important meiotic events including chromosome pairing. Together, these observations of an asymmetrical HS phenotype in intersubspecific F1males, probably owing to meiotic defects in the meiotic behavior of the XY chromosomes pair and possibly also transcriptional misregulation of meiotic genes, provide new models and directions for understanding speciation mechanisms in mammals.