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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >The mouse juvenile spermatogonial depletion (jsd) phenotype is due to a mutation in the X-derived retrogene, mUtp14b.
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The mouse juvenile spermatogonial depletion (jsd) phenotype is due to a mutation in the X-derived retrogene, mUtp14b.

机译：小鼠少年精原细胞耗竭（jsd）表型归因于X衍生逆转录基因mUtp14b中的突变。

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The recessive juvenile spermatogonial depletion (jsd) mutation results in a single wave of spermatogenesis, followed by failure of type A spermatogonia to differentiate, resulting in adult male sterility. We have identified a jsd-specific rearrangement in the mouse homologue of the Saccharomyces cerevisiae gene UTP14, termed mUtp14b. Confirmation that mUtp14b underlies the jsd phenotype was obtained by transgenic bacterial artificial chromosome (BAC) rescue. We also identified a homologous gene on the Mus musculus X chromosome (MMUX) (mUtp14a) that is the strict homologue of the yeast gene, from which the intronless mUtp14b has been derived by retrotransposition. Expression analysis showed that mUtp14b is predominantly expressed in the germ line of the testis from zygotene through round spermatids, whereas mUtp14a, although well expressed in all somatic tissues, could be detected only in the germ line in round spermatids. In yeast, depletion of the UTP proteins impedes production of 18S rRNA, leading to cell death. We propose that the retroposed autosomal copy mUtp14b, having acquired a testis-specific expression pattern, could have provided a mechanism for increasing the efficiency and/or numbers of germ cells produced by meeting the need for more 18S rRNA and protein. Such a mechanism would be of obvious reproductive advantage and be strongly selected for in evolution. Consistent with this hypothesis is the finding of a similar X-autosome retroposition of UTP14 in human which seems to have arisen independently of that in rodents. In jsd homozygotes, which lack a functional copy of Utp14b, insufficient production of rRNA quickly leads to a cessation of spermatogenesis.
机译：隐性的少年精原细胞耗竭（jsd）突变导致单波精子发生，随后导致A型精原细胞无法分化，导致成年男性不育。我们已经在酿酒酵母基因UTP14（称为mUtp14b）的小鼠同源物中鉴定了jsd特异性重排。通过转基因细菌人工染色体（BAC）拯救获得了mUtp14b属于jsd表型的确认。我们还鉴定了小家鼠X染色体（MMUX）（mUtp14a）上的同源基因，该基因是酵母基因的严格同源物，无内含子mUtp14b已通过逆转座子衍生自酵母基因。表达分析表明，mUtp14b主要从合子烯到圆形精子在睾丸生殖系中表达，而mUtp14a尽管在所有体细胞组织中均表达良好，但仅在圆形精子的生殖系中可以检测到。在酵母中，UTP蛋白的消耗会阻止18S rRNA的产生，从而导致细胞死亡。我们建议，已获得睾丸特异性表达模式的逆转常染色体复制mUtp14b，可以提供一种机制，通过满足更多18S rRNA和蛋白质的需求来提高生殖细胞的效率和/或数量。这种机制将具有明显的繁殖优势，并在进化中被强烈选择。与此假设相一致的是，在人体内发现了类似的UTP14 X常染色体逆转，这似乎与啮齿动物无关。在缺乏Utp14b功能性复制的jsd纯合子中，rRNA产生不足会迅速导致精子生成停止。

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