Regional and temporal changes in the pattern of X-chromosome replication during the early post-implantation development of the female mouse

Takagi, Nobuo; Sugawara, Osamu; Sasaki, Masahiko

doi:10.1007/bf00294971

Cited by 173 publications

(113 citation statements)

References 26 publications

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“…However, in the extraembryonic tissues of some placental mammals, such as rodents, XCI takes place in an "imprinted" manner such that the paternal X (Xp) is always silenced (Takagi and Sasaki 1975). Earlier classical cytogenetics studies suggested that the paternal X only becomes inactivated at the blastocyst stage, accompanying cellular differentiation in the trophoectoderm and primitive endoderm (Takagi et al 1982). However, recent studies have revealed that the paternal X has already begun to inactivate by the eight-cell stage (Huynh and Lee 2003;Mak et al 2004;Okamoto et al 2004;Okamoto and Heard 2006) and this inactivation of Xp initiates following Xist RNA coating at the four-cell stage (Okamoto et al 2004(Okamoto et al , 2005.…”

Section: XCImentioning

confidence: 99%

Eukaryotic regulatory RNAs: an answer to the ‘genome complexity’ conundrum

Prasanth¹,

Spector²

2007

Genes Dev.

364

305

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A large portion of the eukaryotic genome is transcribed as noncoding RNAs (ncRNAs). While once thought of primarily as "junk," recent studies indicate that a large number of these RNAs play central roles in regulating gene expression at multiple levels. The increasing diversity of ncRNAs identified in the eukaryotic genome suggests a critical nexus between the regulatory potential of ncRNAs and the complexity of genome organization. We provide an overview of recent advances in the identification and function of eukaryotic ncRNAs and the roles played by these RNAs in chromatin organization, gene expression, and disease etiology.

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Section: XCImentioning

confidence: 99%

Eukaryotic regulatory RNAs: an answer to the ‘genome complexity’ conundrum

Prasanth¹,

Spector²

2007

Genes Dev.

364

305

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“…The first wave occurs during preimplantation embryogenesis and is subject to imprinting, resulting in preferential inactivation of the paternal X (Xp) chromosome (1). Inactivity of the Xp is maintained in the trophectoderm of the blastocyst but is reversed in the inner cell mass (2,3), where a second wave of random XCI takes place, affecting either the Xp or the maternal X (Xm) chromosome (4,5). The initiation of this second wave of XCI is controlled by a key regulatory locus, the X-inactivation center (Xic), which monoallelically upregulates either the paternal or maternal allele of the noncoding Xist transcript, thus triggering XCI in cis during an early time window of differentiation [for review, see Heard and Disteche (6)].…”

mentioning

confidence: 99%

Dynamic changes in paternal X-chromosome activity during imprinted X-chromosome inactivation in mice

Patrat

Okamoto

Diabangouaya

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

155

175

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In mammals, X-chromosome dosage compensation is achieved by inactivating one of the two X chromosomes in females. In mice, X inactivation is initially imprinted, with inactivation of the paternal X (Xp) chromosome occurring during preimplantation development. One theory is that the Xp is preinactivated in female embryos, because of its previous silence during meiosis in the male germ line. The extent to which the Xp is active after fertilization and the exact time of onset of X-linked gene silencing have been the subject of debate. We performed a systematic, single-cell transcriptional analysis to examine the activity of the Xp chromosome for a panel of X-linked genes throughout early preimplantation development in the mouse. Rather than being preinactivated, we found the Xp to be fully active at the time of zygotic gene activation, with silencing beginning from the 4-cell stage onward. X-inactivation patterns were, however, surprisingly diverse between genes. Some loci showed early onset (4 -8-cell stage) of X inactivation, and some showed extremely late onset (postblastocyst stage), whereas others were never fully inactivated. Thus, we show that silencing of some X-chromosomal regions occurs outside of the usual time window and that escape from X inactivation can be highly lineage specific. These results reveal that imprinted X inactivation in mice is far less concerted than previously thought and highlight the epigenetic diversity underlying the dosage compensation process during early mammalian development.dosage compensation ͉ epigenetics ͉ imprinting ͉ mouse development ͉ X inactivation

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“…[144][145][146] Additionally, the Xi has been described, decades ago, to exhibit particular replication dynamics that clearly differ from those of the Xa and the autosomes. 147,148 Hence, the Xi is a particularly interesting example of epigenetic regulation of replication timing. Interesting, the process of facultative heterochromatinization undergone by the Xi and the concomitant changes in replication dynamics, have been proposed to be the most prominent example of what actually happens in many, less prominent, regions of the genome, making the study of the Xi replication dynamics even more relevant.…”

Section: Epigenetics and Dna Replication Timing In Mammalsmentioning

confidence: 99%