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小鼠内源性X连锁基因在发育过程中未表现出谱系特异性的延迟失活。

Mouse endogenous X-linked genes do not show lineage-specific delayed inactivation during development.

作者信息

Lebon J M, Tam P P, Singer-Sam J, Riggs A D, Tan S S

机构信息

Department of Biology, Beckman Research Institute of the City of Hope, Duarte, CA 91010-0269, USA.

出版信息

Genet Res. 1995 Jun;65(3):223-7. doi: 10.1017/s0016672300033292.

Abstract

X chromosome inactivation (XCI) has been assumed to be complete in all cells of female mouse embryos at about 6 d post coitum (dpc). However, a recent study on beta-galactosidase expression of an X-linked lacZ transgene suggests that XCI is probably not complete several days after this time in some lineages. To help resolve this issue, we analysed XCI in embryos which carry the T(X;16)16H (Searle's) translocation and are heterozygous at the X-linked Hprt and Pgk-1 genes. The quantitative RT-PCR single nucleotide primer extension (SNuPE) assay was used to measure Hprt and Pgk-1 allele-specific transcripts in embryos 9.5 dpc. No transcripts from the normal X chromosome were found in any of the tissues tested, indicating that inactivation was complete for these endogenous genes.

摘要

X染色体失活(XCI)被认为在雌性小鼠胚胎受精后约6天(dpc)的所有细胞中已完全完成。然而,最近一项关于X连锁lacZ转基因β-半乳糖苷酶表达的研究表明,在这个时间之后的几天里,某些谱系中的XCI可能并未完全完成。为了帮助解决这个问题,我们分析了携带T(X;16)16H(塞尔氏)易位且在X连锁的Hprt和Pgk-1基因处为杂合子的胚胎中的XCI情况。采用定量逆转录聚合酶链反应单核苷酸引物延伸(SNuPE)分析法来测量9.5 dpc胚胎中Hprt和Pgk-1等位基因特异性转录本。在所测试的任何组织中均未发现来自正常X染色体的转录本,这表明这些内源基因的失活是完全的。

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