Delayed Onset of Replication of Human X Chromosomes

Priest, Jean H.; Heady, Judith E.; Priest, Robert E.

doi:10.1083/jcb.35.2.483

Cited by 65 publications

(23 citation statements)

References 8 publications

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“…The available evidence indicates that the same replication origins are utilized on the active and inactive X chromosomes (Cohen et al 2003;Gomez and Brockdorff 2004), thus suggesting 1 that the replication timing differences between the two X chromosomes stem from the times in S phase that their origins are activated. While in female human cells the Xi is replicated much later in S phase than the Xa (Priest et al 1967), the Xi is not replicated nearly as late in S phase in female mouse cells as in human cells (Evans et al 1965;Galton and Holt 1965;Tiepolo et al 1967). This has led to the Xi in mouse cells being distinguished by its absence of label incorporation in early S phase rather than by its being disproportionately replicated late in S phase (Nesbitt and Gartler 1970).…”

mentioning

confidence: 93%

A Deletion at the MouseXistGene ExposesTrans-effects That Alter the Heterochromatin of the Inactive X Chromosome and the Replication Time and DNA Stability of Both X Chromosomes

Diaz-Perez¹,

Ferguson²,

Wang

et al. 2006

Genetics

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The inactive X chromosome of female mammals displays several properties of heterochromatin including late replication, histone H4 hypoacetylation, histone H3 hypomethylation at lysine-4, and methylated CpG islands. We show that cre-Lox-mediated excision of 21 kb from both Xist alleles in female mouse fibroblasts led to the appearance of two histone modifications throughout the inactive X chromosome usually associated with euchromatin: histone H4 acetylation and histone H3 lysine-4 methylation. Despite these euchromatic properties, the inactive X chromosome was replicated even later in S phase than in wild-type female cells. Homozygosity for the deletion also caused regions of the active X chromosome that are associated with very high concentrations of LINE-1 elements to be replicated very late in S phase. Extreme late replication is a property of fragile sites and the 21-kb deletions destabilized the DNA of both X chromosomes, leading to deletions and translocations. This was accompanied by the phosphorylation of p53 at serine-15, an event that occurs in response to DNA damage, and the accumulation of g-H2AX, a histone involved in DNA repair, on the X chromosome. The Xist locus therefore maintains the DNA stability of both X chromosomes.

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mentioning

confidence: 93%

A Deletion at the MouseXistGene ExposesTrans-effects That Alter the Heterochromatin of the Inactive X Chromosome and the Replication Time and DNA Stability of Both X Chromosomes

Diaz-Perez¹,

Ferguson²,

Wang

et al. 2006

Genetics

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“…Compared to the autosomes and its homolog, the inactive X chromosome is characterized by several features, such as its strong compaction at interphase, forming the Barr body (Barr and Carr, 1961), its late replication in S-phase (Gilbert et al, 1962;Morishima et al, 1962;Priest et al, 1967), its stainability (Kanda, 1973;Kanda and Yosida, 1979;Bernardino-Sgherri and Dutrillaux, 2001), and its condensation at metaphase (Takagi and Oshimura, 1973;Haaf et al, 1993;Bernardino-Sgherri and Dutrillaux, 2001).…”

mentioning

confidence: 99%

Overall DNA methylation and chromatin structure of normal and abnormal X chromosomes

Bernardino-Sgherri

Flagiello

Dutrillaux

2002

Cytogenet Genome Res

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DNA methylation patterns were studied at the chromosome level in normal and abnormal X chromosomes using an anti-5-methylcytosine antibody. In man, except for the late-replicating X of female cells, the labeled chromosome structures correspond to R- and T-bands and heterochromatin. Depending on the cell type, the species, and cell culture conditions, the late-replicating X in female cells appears to be more or less undermethylated. Under normal conditions, the only structures that remain methylated on the X chromosomes correspond to pseudoautosomal regions, which harbor active genes. Thus, active genes are usually hypomethylated but are located in methylated chromatin. Structural rearrangements of the X chromosome, such as t(X;X)(pter;pter), induce a Turner syndrome-like phenotype that is inconsistent with the resulting triple-X constitution. This suggests a position effect controlling gene inactivation. The derivative chromosomes are always late replicating, and their duplicated short arms, which harbor pseudoautosomal regions, replicate later than the normal late-replicating X chromosomes. The compaction or condensation of this segment is unusual, with a halo of chromatin surrounding a hypocondensed chromosome core. The chromosome core is hypomethylated, but the surrounding chromatin is slightly labeled. Thus, unusual DNA methylation and chromatin condensation are associated with the observed position effect. This strengthens the hypothesis that DNA methylation at the chromosome level is associated with both chromatin structure and gene expression.

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“…This revealed that the latest replicating portions of the genome were disproportionately on one of the two X chromosomes in diploid cells (Figure 1,C and D). In female human cells the Xi is replicated considerably later in S phase than the Xa (Priest et al 1967). In female mouse cells, the Xi is not replicated as late in S phase as it is in human cells (Evans et al 1965;Galton and Holt 1965;Tiepolo et al 1967).…”

Section: Resultsmentioning

confidence: 86%

The Element(s) at the Nontranscribed Xist Locus of the Active X Chromosome Controls Chromosomal Replication Timing in the Mouse

et al. 2005

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In female mammalian cells, the inactive X chromosome is replicated late in S phase while the active X chromosome is replicated earlier. The replication times of the X chromosomes reflect a general trend in which late replication is associated with gene repression and earlier replication with transcriptional competence. The X-linked Xist gene is expressed exclusively from the inactive X chromosome where it is involved in the initiation and maintenance of X-inactivation. In contrast, no biological activity has been assigned to the Xist locus of the active X chromosome where the Xist gene is transcriptionally silenced. Here, we provide evidence that the element(s) at the nontranscribed Xist locus of the active X chromosome controls chromosomal replication timing in cis.

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Delayed Onset of Replication of Human X Chromosomes

Cited by 65 publications

References 8 publications

A Deletion at the MouseXistGene ExposesTrans-effects That Alter the Heterochromatin of the Inactive X Chromosome and the Replication Time and DNA Stability of Both X Chromosomes

A Deletion at the MouseXistGene ExposesTrans-effects That Alter the Heterochromatin of the Inactive X Chromosome and the Replication Time and DNA Stability of Both X Chromosomes

Overall DNA methylation and chromatin structure of normal and abnormal X chromosomes

The Element(s) at the Nontranscribed Xist Locus of the Active X Chromosome Controls Chromosomal Replication Timing in the Mouse

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