Isolation and characterization of alphoid DNA sequences specific for the pericentric regions of chromosomes 4, 5, 9, and 19

Hulsebos, Theo J.M.; Schonk, D.; Dalen, Ineke van; Coerwinkel-Driessen, M.; Schepens, Jan; Ropers, H.-H.; Wieringa, B.

doi:10.1159/000132533

Cited by 40 publications

(25 citation statements)

References 7 publications

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“…FISH probes were pG-A16 (D5Z1) (Hulsebos et al, 1988), pZ5.1 (D5Z2) (Archidiacono et al, 1995), D7Z1 (p7t1) (Waye et al, 1987), D7Z2 (pMGB7) (Waye et al, 1987), GDNF (Schindelhauer et al, 1995) or commercial CEP 17 and CEP X probes (Abbot Molecular, Des Plaines, IL, USA). DNA was counterstained with DAPI.…”

Section: Chromatin Immunoprecipitation and Pcrmentioning

confidence: 99%

Cancer-associated alteration of pericentromeric heterochromatin may contribute to chromosome instability

et al. 2011

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Many tumors exhibit elevated chromosome mis-segregation termed chromosome instability (CIN), which is likely to be a potent driver of tumor progression and drug resistance. Causes of CIN are poorly understood but probably include prior genome tetraploidization, centrosome amplification and mitotic checkpoint defects. This study identifies epigenetic alteration of the centromere as a potential contributor to the CIN phenotype. The centromere controls chromosome segregation and consists of higher-order repeat (HOR) alpha-satellite DNA packaged into two chromatin domains: the kinetochore, harboring the centromere-specific H3 variant centromere protein A (CENP-A), and the pericentromeric heterochromatin, considered important for cohesion. Perturbation of centromeric chromatin in model systems causes CIN. As cancer cells exhibit widespread chromatin changes, we hypothesized that pericentromeric chromatin structure could also be affected, contributing to CIN. Cytological and chromatin immunoprecipitation and PCR (ChIP-PCR)-based analyses of HT1080 cancer cells showed that only one of the two HORs on chromosomes 5 and 7 incorporate CENP-A, an organization conserved in all normal and cancer-derived cells examined. Contrastingly, the heterochromatin marker H3K9me3 (trimethylation of H3 lysine 9) mapped to all four HORs and ChIP-PCR showed an altered pattern of H3K9me3 in cancer cell lines and breast tumors, consistent with a reduction on the kinetochore-forming HORs. The JMJD2B demethylase is overexpressed in breast tumors with a CIN phenotype, and overexpression of exogenous JMJD2B in cultured breast epithelial cells caused loss of centromere-associated H3K9me3 and increased CIN. These findings suggest that impaired maintenance of pericentromeric heterochromatin may contribute to CIN in cancer and be a novel therapeutic target.

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Section: Chromatin Immunoprecipitation and Pcrmentioning

confidence: 99%

Cancer-associated alteration of pericentromeric heterochromatin may contribute to chromosome instability

et al. 2011

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“…A 3 kb unique sequence insert isolated from ECB27 was used for tritium labeling. Probe pG-A16 was a 1.95 kb insert in a plasmid vector, which hybridizes strongly to the pericentric regions of chromosomes 5 and 19 (Hulsebos et al, 1988).…”

Section: Probesmentioning

confidence: 99%

Fine Mapping of Probes in the Adenomatous Polyposis Coli Region of Chromosome 5 by In Situ Hybridization

Williams

Jones

Cottrell

et al. 1991

Genes Chromosomes & Cancer

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The gene for adenomatous polyposis coli has been localized to 5q21-22. We have mapped six probes from this region using isotopic or nonisotopic in situ hybridization. Using tritium-labeled probes we localized II227 (D5S37) to 5q14-15 and ECB27 (D5S98) to 5q21. Following hybridization with biotin-labeled probes, the positions of signals along the chromosomes were measured as fractional length relative to the length of the chromosome arm from centromere to qter (FLcen-qter). Ninety-five percent confidence limits, compared with standard karyotypes, provided the corresponding band localization. By this method we localized Cllpll (D5S71) to FLcen-qter 0.407-0.452 (5q21.1-21.3), ECB27 to FLcen-qter 0.426-0.473 (5q21.3), YN5.48 (D5S81) to FLcen-qter 0.459-0.496 (5q21.3-22.2), and ECB134 (D5S97) to FLcen-qter 0.509-0.533 (5q22.3-23.1). ECB220 had three sites of hybridization, a major site at FLcen-qter 0.460-0.492 (5q21.3-22.1) and minor sites at FLcen-qter 0.299-0.339 (5q14.3-15) and FLcen-qter 0.629-0.691 (5q23.3-31.2). We have shown that the chromosome 5 breakpoint in a t(5;15) translocation from a patient with Gardner's syndrome (GM03314) is between Cllpll and ECB27. Linkage data are presented suggesting that ECB27 is located on the same side of the APC locus as II227. These and published results including data on several constitutional deletions (M, SD, and brothers PW and ND) give a probable order of [cen] - [II227, proximal SD breakpoint] - [Cllpll] - [proximal PW/ND, M breakpoint(s), GM03314 breakpoint] - [ECB27] - [APC] - [YN5.48] - [distal PW/ND breakpoint] - [ECB134] - [distal M breakpoint] - [qter]. The major site of ECB220 appears to be between ECB27 and the distal PW/ND breakpoint; the distal SD breakpoint is distal to YN5.48.

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“…Three different satellite DNA probes characterizing the centromeric and pericentromeric regions of chromosome 9 were used: an alphoid DNA sequence (probe pG-Xb11/340) binding specifically to the centromere of chromosomes 4 and 9 [Hulsebos et al, 1988], a chromosome 9-specific beta satellite probe (ONCOR. Gaithersburg, MD; D9Z5) and a chromosome 9-specific classical satellite III probe (ONCOR; D9Z1), specific for the proximal and distal parts, respectively, of the heterochromatic secondary constriction (Fig.…”

Section: Chromosome Studiesmentioning

confidence: 99%

“…Molecular cytogenetic techniques have now unequivocally shown that the region including the centromere and the secondary constriction of the normal chromosome 9 is mainly composed of three spatially distinct and specifically ranged domains of repeated satellite DNA sequences, namely, alpha, beta, and classical satellite III DNA [Singer, 1982;Hulsebos et al, 1988;Waye and Willars, 1989;Choo et al, 1991;Rocchi et al, 1991;Luke et al, 1992;Cook and Karpen, 1994;Haaf and Ward, 1994;Ramesh and Verma, 1996].…”

Section: Introductionmentioning

confidence: 99%

Dicentric chromosome 9 due to tandem duplication of the 9p11-q13 region: Unusual chromosome 9 variant

2000

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We report on a 31-year-old mentally retarded woman with minor facial anomalies and a heteromorphic chromosome 9 with tandem duplication of the 9p11-q13 pericentromeric region. To the best of our knowledge, this is the first report of tandem duplication of this region. An identical chromosome 9 morphology was found in the healthy and phenotypically normal sister of the proposita. The usefulness of double-color FISH techniques and the presumed mechanism accounting for the origin of the chromosomal anomaly and for the phenotypic discordance observed between the two sisters are discussed.

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Isolation and characterization of alphoid DNA sequences specific for the pericentric regions of chromosomes 4, 5, 9, and 19

Cited by 40 publications

References 7 publications

Cancer-associated alteration of pericentromeric heterochromatin may contribute to chromosome instability

Cancer-associated alteration of pericentromeric heterochromatin may contribute to chromosome instability

Fine Mapping of Probes in the Adenomatous Polyposis Coli Region of Chromosome 5 by In Situ Hybridization

Dicentric chromosome 9 due to tandem duplication of the 9p11-q13 region: Unusual chromosome 9 variant

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