Expression of Xist during mouse development suggests a role in the initiation of X chromosome inactivation

Kay, Graham F.; Penny, Graeme D.; Patel, Dipika V.; Ashworth, Alan; Brockdorff, Neil; Rastan, Sohaila

doi:10.1016/0092-8674(93)90658-d

Cited by 344 publications

(236 citation statements)

References 45 publications

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“…Previous studies had suggested that genes may be expressed at a lower level from the X p in preimplantation embryos. (11)(12)(13) The current papers (1)(2)(3) that we discuss here further challenge the view that both X chromosomes are expressed in early stages of development by providing clear evidence of X p inactivation in preimplantation embryos.…”

Section: Introductionmentioning

confidence: 76%

“…(11,14,15) Xist RNA expression first appears at the 2-to 4-cell stage and this early expression of Xist is exclusively of paternal origin. (11) To follow early changes in global X-linked gene expression in mouse preimplantation embryos, Huynh and Lee used RNA fluorescence in situ hybridization (RNA-FISH) with a Cot-1 probe together with an Xist probe. (1) Active transcription as measured by the Cot-1 signal was first detected at the 2-cell stage, which is when zygotic gene activation commences.…”

Section: Introductionmentioning

confidence: 99%

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Silence of the fathers: Early X inactivation

Cheng

Distèche

2004

BioEssays

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Section: Introductionmentioning

confidence: 76%

Section: Introductionmentioning

confidence: 99%

Silence of the fathers: Early X inactivation

Cheng

Distèche

2004

BioEssays

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“…The paternal X chromosome is selectively inactivated by imprinting in the extra-embryonic tissues, which give rise to the placenta and part of the extra-embryonic membranes (Takagi and Sasaki, 1975), where the paternal copy of Xist is always activated and the maternal one is never expressed (Kay et al, 1993). Targeted disruption of Tsix, when maternally inherited, induces ectopic activation of the normally silent copy of Xist on the same X chromosome in these tissues (Lee, 2000;Sado et al, 2001).…”

Section: Introductionmentioning

confidence: 99%

Tsixdefective in splicing is competent to establishXistsilencing

2006

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Dosage differences of X-linked genes between male and female mammals are compensated for by a mechanism known as Xinactivation, and the noncoding Xist gene plays a crucial role in this process. The expression of Xist is regulated in cis by its noncoding antisense gene, Tsix, whose transcripts (though a fraction of them stay unspliced), are processed like common proteincoding RNAs. It has been suggested that certain classes of sense-antisense pairs of RNA are causally involved in not only gene regulation but also higher order chromatin structure in various organisms. In fact, recent studies demonstrated that Tsix modulates Xist expression through modification of the chromatin structure. It is still unknown, however, whether the RNA product is important for the function of Tsix or whether the antisense transcription is sufficient. To obtain insight into this issue, we eliminated the splicing products of Tsix in the mouse and explored the effects of this elimination on Tsix-mediated Xist silencing. To our surprise, the Xist locus was stably repressed on the X carrying the splicing-defective Tsix allele. Moreover, the repressive chromatin configuration was properly established at the Xist locus. These unexpected results indicate that the splicing products are dispensable for Tsix-mediated Xist silencing.

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“…Furthermore, imprinted genes are frequently linked within clusters that contain both maternally and paternally expressed genes (Zemel et al 1992;Mutirangura et al 1993;Rougeulle et al 1997;Vu and Hoffmann 1997;Wutz et al 1997). Finally, an unusual feature of these clusters is that they contain at least one imprinted gene that encodes an untranslated RNA (Brannan et al 1990;Kay et al 1993;Wevrick et al 1994;Wutz et al 1997).…”

mentioning

confidence: 99%

Igf2 imprinting does not require its own DNA methylation or H19 RNA

Jones

Levorse²,

Tilghman³

1998

Genes Dev.

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Three models have been proposed to explain the imprinting of the mouse Igf2 gene on the maternal chromosome. We ruled out the importance of DNA methylation at Igf2 by showing that silencing of Igf2 accompanying the loss of DNA methylation could be overcome by a mutation at the neighboring H19 gene that activates Igf2. By replacing the H19 structural gene with a protein-coding gene, we have ruled out a role for H19 RNA in the imprinting of Igf2. This replacement resulted in sporadic activation of the H19 promoter on the paternal chromosome without affecting the level of expression of Igf2, a finding that is inconsistent with strict promoter competition between the genes. We conclude that a transcriptional model involving access to a common set of enhancers shared between Igf2 and H19 is the most likely explanation for Igf2 imprinting.

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Expression of Xist during mouse development suggests a role in the initiation of X chromosome inactivation

Cited by 344 publications

References 45 publications

Silence of the fathers: Early X inactivation

Silence of the fathers: Early X inactivation

Tsixdefective in splicing is competent to establishXistsilencing

Igf2 imprinting does not require its own DNA methylation or H19 RNA

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