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首页> 外文期刊>Current Biology: CB >Satellite Repeats Identify X Chromatin for Dosage Compensation in Drosophila melanogaster Males
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Satellite Repeats Identify X Chromatin for Dosage Compensation in Drosophila melanogaster Males

机译：卫星重复鉴定曲霉素曲霉素用于果蝇melanogaster男性的剂量补偿

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A common feature of sex chromosomes is coordinated regulation of X-linked genes in one sex. Drosophila melanogaster males have one X chromosome, whereas females have two. The resulting imbalance in gene dosage is corrected by increased expression from the single X chromosome of males, a process known as dosage compensation. In flies, compensation involves recruitment of the male-specific lethal (MSL) complex to X-linked genes and modification of chromatin to increase expression. The extraordinary selectivity of the MSL complex for the X chromosome has never been explained. We previously demonstrated that the small interfering RNA (siRNA) pathway and siRNA from a family of X-linked satellite repeats (1.688(X) repeats) promote X recognition. Now, we test the ability of 1.688(X) DNA to attract compensation to genes nearby and report that autosomal integration of 1.688(X) repeats increases MSL recruitment and gene expression in surrounding regions. Placement of 1.688(X) repeats opposite a lethal autosomal deletion achieves partial rescue of males, demonstrating functional compensation of autosomal chromatin. Females block formation of the MSL complex and are not rescued. The 1.688(X) repeats are therefore cis-acting elements that guide dosage compensation. Furthermore, 1.688(X) siRNA enhances rescue of males with a lethal deletion but only when repeat DNA is present on the intact homolog. We propose that the siRNA pathway promotes X recognition by enhancing the ability of 1.688(X) DNA to attract compensation in cis. The dense and near-exclusive distribution of 1.688(X) sequences along the X chromosome suggests that they play a primary role in determining X identity during dosage compensation.
机译：性染色体的常见特征是在一种性别中对X链接基因的协调调节。果蝇黑色素醛母亲有一个X染色体，而女性有两个。通过从单一X染色体的表达增加，校正基因剂量的产生的不平衡，该方法称为剂量补偿。在苍蝇中，补偿涉及募集致癌基因的男性特异性致死（MSL）复合物和染色质的修饰以增加表达。从未解释过X染色体的MSL复合物的非凡选择性。我们之前证明，来自X型卫星卫星系列的小型干扰RNA（siRNA）途径和siRNA（1.688（x）重复）促进X识别。现在，我们测试1.688（x）DNA的能力，以吸引附近的基因补偿，并报告的是1.688（x）重复的常染色体一体化增加了周围地区的MSL募集和基因表达。 1.688（x）的放置重复对面的致死常染色体缺失，实现了雄性的部分拯救，证明了常染色体染色质的功能性补偿。女性阻止MSL复合体的形成，并且不会救出。因此，1.688（X）重复是CIS作用元素，指导剂量补偿。此外，1.688（x）siRNA增强了致命缺失的雄性拯救，但只有当重复DNA存在于完整同源物上时。我们提出siRNA途径通过提高1.688（X）DNA吸引顺式补偿的能力来促进X识别。沿X染色体的1.688（x）序列的致密和接近独占分布表明它们在剂量补偿期间确定X身份起着主要作用。

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    《Current Biology: CB》 |2017年第10期|共12页
  • 作者

    Joshi Sonal S.; Meller Victoria H.;

  • 作者单位

    Wayne State Univ Dept Biol Sci 5047 Gullen Mall Detroit MI 48020 USA;

    Wayne State Univ Dept Biol Sci 5047 Gullen Mall Detroit MI 48020 USA;

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  • 正文语种 eng
  • 中图分类 生物科学;
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