Enhanced expression in seminoma of human zinc finger genes located on chromosome 19

Ogawa, Takehiko; Poncelet, Dominique; Kinoshita, Yuzo; Noce, Toshiaki; Takeda, Mitsumasa; Kawamoto, Kanji; Udagawa, Koichi; Lecocq, P J; Marine, Jean–Christophe; Martial, Joseph; Hosaka, Masahiko

doi:10.1016/s0165-4608(97)00004-6

Cited by 9 publications

(5 citation statements)

References 22 publications

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“…Instead, a high level of background (multiple weak hybridization signals of ∼1.0 kb and 4.2, 4.4, and 5.0 kb) was observed in most tissues examined. Such weak background hybridization signals have been reported previously for several ZNF genes (Derry et al 1995;Baban et al 1996;Ogawa et al 1998) and, as has been suggested, likely represent a combination of low-level expression and cross-hybridization from multiple members of the KRAB-ZNF gene family. To eliminate the problem of background hybridization and to specifically test for each of the two ZNF208 isoforms, a specific RT-PCR assay was developed for each of the two alternative transcripts of the ZNF208 gene (Fig.…”

Section: Expression Analysissupporting

confidence: 78%

Complex β-Satellite Repeat Structures and the Expansion of the Zinc Finger Gene Cluster in 19p12

et al. 1998

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We investigated the organization, architecture, and evolution of the largest cluster (∼4 Mb) of Krüppel-associated box zinc finger (KRAB-ZNF) genes located in cytogenetic band interval 19p12. A highly integrated physical map (∼700 kb) of overlapping cosmid and BAC clones was developed between genetic STS markers D19S454 and D19S269. Using ZNF91 exon-specific probes to interrogate a detailed EcoRI restriction map of the region, ZNF genes were found to be distributed in a head-to-tail fashion throughout the region with an average density of one ZNF duplicon every 150-180 kb of genomic distance. Sequence analysis of 208,967 bp of this region indicated the presence of two putative ZNF genes: one consisting of a novel member of this gene family (ZNF208) expressed ubiquitously in all tissues examined and the other representing a nonprocessed pseudogene (ZNF209), located 450 kb proximal to ZNF208. Large blocks of (∼25-kb) inverted ␤-satellite repeats with a remarkably symmetrical higher order repeat structure were found to bracket the functional ZNF gene. Hybridization analysis using the ␤-satellite repeat as a probe indicates that ␤-satellite interspersion between ZNF gene cassettes is a general property for 1.5 Mb of the ZNF gene cluster in 19p12. Both molecular clock data as well as a retroposon-mapping molecular fossil approach indicate that this ZNF cluster arose early during primate evolution (∼50 million years ago). We propose an evolutionary model in which heteromorphic pericentromeric repeat structures such as the ␤ satellites have been coopted to accommodate rapid expansion of a large gene family over a short period of evolutionary time.[The sequence data described in this paper have been submitted to GenBank under accession nos. AC003973 and AC004004.] Zinc finger (ZNF) genes represent one of the largest gene families in the human genome with an estimated 500-600 members (Hoovers et al. 1992;Becker et al. 1995;Klug and Schwabe 1995). Although the specific function of the majority of ZNF genes remains largely unknown, as a class they are believed to encode transcriptional regulators that in a few instances have been shown to play critical roles in cellular and developmental differentiation processes (Pieler and Bellefroid 1994). ZNF proteins have been implicated in many diverse eukaryotic developmental processes, such as segment pattern formation in the Drosophila embryo (Rosenberg et al. 1986); cellular proliferation in the cerebellar hindbrain of the mouse (Wilkinson et al. 1989); and hematopoietic differentiation among human myeloid precursor cells (Hromas et al. 1991). DNA binding of the encoded proteins is typically mediated by a ZNF motif that consists either of two cysteines and two histidines (Krüppel family or C 2 /H 2 type) or four cysteines alone (steroid receptor or C 2 / C 2 type). The conserved cysteines and/or histidines form a tetrahedral complex around a zinc metal ion, generating a folded loop or ''finger'' of 30 amino acids that is capable of making contact with DNA (Miller et al. 1985)...

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Section: Expression Analysissupporting

confidence: 78%

Complex β-Satellite Repeat Structures and the Expansion of the Zinc Finger Gene Cluster in 19p12

et al. 1998

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“…For example, an isochromosome 12p and de®ciencies in the short arms of chromosomes 1, 3, and 11 are concurrent with TGCTs (reviewed in Looijenga et al, 1999a;Looijenga and Oosterhuis, 1999b), implicating the presence of potential TGCT suppressor genes in these de®ciency regions. Recently, seminomas have also been correlated to the altered activities of speci®c genes such as glial cell line-derived neurotrophic factor (GDNF), members of placental alkaline phosphatase family, Zinc ®nger genes on chromosome 19, eukaryotic initiation factor 3 p110 mRNA, and Testis Speci®c Protein Y Encoded (TSPY; Ogawa et al, 1998;Rothe et al, 2000;Lau et al, 2000;Meng et al, 2001;Shigenari et al, 1998). Despite these progresses, the genetic mechanism that leads to the pathenogenesis of seminomas remains elusive.…”

Section: Introductionmentioning

confidence: 99%

Molecular characterization of hiwi, a human member of the piwi gene family whose overexpression is correlated to seminomas

et al. 2002

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“…Further analysis shows that 30 of the 136 upregulated genes are zinc finger (ZF) proteins belonging to the Krueppel C2H2‐type ZF protein family. Almost all of these upregulated ZF proteins (27 of 30) are located together on chromosome 19 (Supporting Information Table S4) and were previously found to be upregulated in seminomas [48, 49]. Interestingly, Hittmair et al [50] showed that a subpopulation of seminomas express CD30 and that CD30 expression in seminomas might indicate their upcoming transformation to embryonal carcinoma.…”

Section: Resultsmentioning

confidence: 97%

Ascorbate Promotes Epigenetic Activation of CD30 in Human Embryonic Stem Cells

et al. 2010

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Human embryonic stem cells (hESCs) and induced pluripotent stem cells have the ability to adapt to various culture conditions. Phenotypic and epigenetic changes brought about by the culture conditions can, however, have significant impacts on their use in research and in clinical applications. Here, we show that diploid hESCs start to express CD30, a biomarker for malignant cells in Hodgkin's disease and embryonal carcinoma cells, when cultured in knockout serum replacement (KOSR)-based medium, but not in fetal calf serum containing medium. We identify the commonly used medium additive, ascorbate, as the sole medium component in KOSR responsible for CD30 induction. Our data show that this epigenetic activation of CD30 expression in hESCs by ascorbate occurs through a dramatic loss of DNA methylation of a CpG island in the CD30 promoter. Analysis of the phenotype and transcriptome of hESCs that overexpress the CD30 signaling domain reveals that CD30 signaling leads to inhibition of apoptosis, enhanced single-cell growth, and transcriptome changes that are associated with cell signaling, lipid metabolism, and tissue development. Collectively, our data show that hESC culture media that contain ascorbate trigger CD30 expression through an epigenetic mechanism and that this provides a survival advantage and transcriptome changes that may help adapt hESCs to in vitro culture conditions.

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Enhanced expression in seminoma of human zinc finger genes located on chromosome 19

Cited by 9 publications

References 22 publications

Complex β-Satellite Repeat Structures and the Expansion of the Zinc Finger Gene Cluster in 19p12

Complex β-Satellite Repeat Structures and the Expansion of the Zinc Finger Gene Cluster in 19p12

Molecular characterization of hiwi, a human member of the piwi gene family whose overexpression is correlated to seminomas

Ascorbate Promotes Epigenetic Activation of CD30 in Human Embryonic Stem Cells

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