Transient homologous chromosome pairing marks the onset of X inactivation
Transient homologous chromosome pairing marks the onset of X inactivation
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DOI：
10.1126/science.1122984
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发表时间：
2006-02-24
期刊：
影响因子：
56.9
通讯作者：
Lee, JT
中科院分区：
文献类型：
--
作者：
Xu, N;Tsai, CL;Lee, JT
哺乳动物X染色体失活关闭了一条雌性X染色体，以在XX和XY个体之间进行剂量补偿。已知X失活由Xite、Tsix和Xist顺式调节，但原则上这两个X也必须反式调节以确保相互排斥的沉默。在这里，我们证明了染色体间配对介导这种通信。配对在X失活开始时短暂发生，并且对X失活中心具有特异性。删除Xite和Tsix干扰配对和计数/选择，而它们的常染色体插入诱导从头X-常染色体配对。异位X-常染色体相互作用抑制内源性X-X配对并阻断X-染色体失活的起始。因此，Tsix和Xite的功能都在顺式和反式。我们建议，Tsix和Xite调节计数和互斥的选择，通过X-X配对。
Mammalian X inactivation turns off one female X chromosome to enact dosage compensation between XX and XY individuals. X inactivation is known to be regulated in cis by Xite, Tsix, and Xist, but in principle the two Xs must also be regulated in trans to ensure mutually exclusive silencing. Here, we demonstrate that interchromosomal pairing mediates this communication. Pairing occurs transiently at the onset of X inactivation and is specific to the X-inactivation center. Deleting Xite and Tsix perturbs pairing and counting/choice, whereas their autosomal insertion induces de novo X-autosome pairing. Ectopic X-autosome interactions inhibit endogenous X-X pairing and block the initiation of X-chromosome inactivation. Thus, Tsix and Xite function both in cis and in trans. We propose that Tsix and Xite regulate counting and mutually exclusive choice through X-X pairing.