YAC clone contigs covering 5 Mb of a repeat sequence island on the mouse X Chromosome

Mileham, P.; Brown, S. D. M.

doi:10.1007/s003359900077

Cited by 4 publications

(2 citation statements)

References 24 publications

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“…This result is consistent with previously published cytogenetic and immunoprecipitation analyses (22,36). The DXSmh141 probe, corresponding to a long complex repeat unit sequence island located in the Giemsa-positive A3 band on the mouse X chromosome (28,37), also hybridizes predominantly to the antibody unbound (hypoacetylated) chromatin fraction. This observation concurs with cytogenetic analysis of histone H4 acetylation levels that suggest that late-replicating Giemsanegative bands are hypoacetylated (36).…”

Section: Resultssupporting

confidence: 81%

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Chromatin structure analysis of the mouse Xist locus

McCabe

Formstone²,

O’Neill³

et al. 1999

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

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The Xist gene is expressed exclusively from the inactive X chromosome and plays a central role in regulating X chromosome inactivation. Here we describe experiments aimed at defining the extent of the active chromatin domain of the expressed Xist allele. By using an allelespecific general DNaseI sensitivity assay we show that there is preferential digestion of the expressed allele at sites within the transcribed locus but not in f lanking sites located up to 70 kb 5. A putative proximal boundary for the Xist domain is located within 10 kb upstream of promoter P 1 . Chromatin in the expressed domain was found to be acetylated at H4 in XX somatic cells but also in XY cells, where Xist is never expressed. A single clear exception to this was the Xist promoter, which is acetylated only in XX cells. These observations concur with the view that H4 acetylation may not be a general marker of active chromatin domains and further support data implicating local promoter acetylation as being of primary functional significance in vivo.In female mammals, dosage compensation is achieved by the transcriptional silencing of one of the two X chromosomes, a process known as X inactivation (1). Features of the inactive X chromosome (Xi) that distinguish it from its active counterpart (Xa) are that it is condensed during interphase, replicates late in S phase, and is underacetylated at histones H3 and H4 (reviewed in ref. 2). More recently it has been shown that chromatin on Xi is highly enriched for the variant histone macroH2A (3).The classically defined X inactivation center (Xic) is required both for initiation of X inactivation in early development and for propagation of the inactivation signal in cis (reviewed in ref. 4). Initiation of random X inactivation involves determining how many (counting) and which (choosing) X chromosome to inactivate. It has been suggested that this is achieved by cells blocking a single Xic and thus marking that chromosome as the active X chromosome. X inactivation then proceeds in cis from unblocked Xics at the onset of cellular differentiation (5).The X inactive specific transcript (Xist) gene, originally identified as a candidate for the Xic (6-9), produces a large RNA with no apparent protein coding potential (10, 11). Xist RNA ''coats'' the inactive X chromosome domain in the interphase nucleus, suggesting that it provides the primary signal for in cis propagation of X inactivation (11,12). A requirement for Xist in propagation of X inactivation in cis has been demonstrated by using targeted deletion of transcribed regions (13,14). Importantly, the counting function of the Xic was unaffected in these experiments. A subsequent genetargeting experiment indicated that sequences distal to Xist are important in counting (15). Analysis of XY embryonic stem (ES) cells bearing a 450-kb Xist yeast artificial chromosome transgene demonstrated that Xist is sufficient for X inactivation (16) and that transgenic loci recapitulate both counting and propagation functions (16,17). This result was subs...

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Section: Resultssupporting

confidence: 81%

“…33H(2) is a 2-kb HindIII genomic fragment located between the E55(16) probe and DXCrc318. Other probes are as described; Xist cDNA clones mXist1, w5i and w7d (8,10); NM18B (23); Cdx4 exon 3 region (24); Tsx (25); actin cDNA clone (26); R198 mouse minor satellite probe (27); DXSmh141 probe (28).…”

mentioning

confidence: 99%

Chromatin structure analysis of the mouse Xist locus

McCabe

Formstone²,

O’Neill³

et al. 1999

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

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Physical Mapping of the Mouse Genome

Herman

1998

Methods

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Heritable gene silencing in lymphocytes delays chromatid resolution without affecting the timing of DNA replication

et al. 2003

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Temporal control of DNA replication has been implicated in epigenetic regulation of gene expression on the basis of observations that certain tissue-specific genes replicate earlier in expressing than non-expressing cells. Here, we show evidence that several leukocyte-specific genes replicate early in lymphocytes regardless of their transcription and also in fibroblasts, where these genes are never normally expressed. Instead, the heritable silencing of some genes (Rag-1, TdT, CD8alpha and lambda5) and their spatial recruitment to heterochromatin domains within the nucleus of lymphocytes resulted in a markedly delayed resolution of sister chromatids into doublet signals discernable by 3D fluorescence in situ hybridization (FISH). Integration of transgenes within heterochromatin (in cis) did, however, confer late replication and this was reversed after variegated transgene expression. These findings emphasise that chromosomal location is important for defining the replication timing of genes and show that retarded sister-chromatid resolution is a novel feature of inactive chromatin.

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YAC clone contigs covering 5 Mb of a repeat sequence island on the mouse X Chromosome

Cited by 4 publications

References 24 publications

Chromatin structure analysis of the mouse Xist locus

Chromatin structure analysis of the mouse Xist locus

Physical Mapping of the Mouse Genome

Heritable gene silencing in lymphocytes delays chromatid resolution without affecting the timing of DNA replication

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