X chromosome inactivation during Drosophila spermatogenesis

X chromosome inactivation during Drosophila spermatogenesis
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DOI:
10.1371/journal.pbio.0050273
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发表时间:
2007-10-01
期刊:
影响因子:
9.8
通讯作者:
Parsch, John
Parsch, John
中科院分区:
生物学1区
文献类型:
--
作者:
Hense, Winfried;Baines, John F.;Parsch, John

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具有雄性和睾丸富集表达的基因在果蝇X染色体上表达不足。还有过量的逆转录转座基因,其中许多在睾丸中表达,它们已经“逃离”X染色体并转移到常染色体。有人提出,在精子发生过程中X染色体的失活有助于这些模式:在精子发生后期具有有益功能的基因应选择性地倾向于常染色体,以避免失活。然而,在男性生殖系中X失活的确凿证据一直缺乏。为了测试这种失活,我们使用了转基因构建体,其中lacZ报告基因的表达由常染色体睾丸特异性ocnus基因的启动子序列驱动。该转基因的常染色体插入显示出预期的雄性和睾丸特异性表达模式。与此相反,X-连锁插入,只显示非常低水平的报告基因表达。因此,我们发现X连锁抑制了睾丸特异性启动子的活性。我们使用转基因两侧为染色体绝缘子序列的载体获得了相同的结果。这些结果与男性生殖系中X染色体的整体失活一致,并支持对X染色体避免在精子发生后期具有有益作用的基因的选择性解释。
Genes with male- and testis-enriched expression are under-represented on the Drosophila melanogaster X chromosome. There is also an excess of retrotransposed genes, many of which are expressed in testis, that have "escaped'' the X chromosome and moved to the autosomes. It has been proposed that inactivation of the X chromosome during spermatogenesis contributes to these patterns: genes with a beneficial function late in spermatogenesis should be selectively favored to be autosomal in order to avoid inactivation. However, conclusive evidence for X inactivation in the male germline has been lacking. To test for such inactivation, we used a transgenic construct in which expression of a lacZ reporter gene was driven by the promoter sequence of the autosomal, testis-specific ocnus gene. Autosomal insertions of this transgene showed the expected pattern of male-and testis-specific expression. X-linked insertions, in contrast, showed only very low levels of reporter gene expression. Thus, we find that X linkage inhibits the activity of a testis-specific promoter. We obtained the same result using a vector in which the transgene was flanked by chromosomal insulator sequences. These results are consistent with global inactivation of the X chromosome in the male germline and support a selective explanation for X chromosome avoidance of genes with beneficial effects late in spermatogenesis.