Cohesin ties up the genome

Carretero, María; Remeseiro, Silvia; Losada, Ana

doi:10.1016/j.ceb.2010.07.004

Cited by 24 publications

(20 citation statements)

References 75 publications

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“…CTCF and cohesins have been implicated in DNA loop interactions (22,54,55). Long-distance DNA interactions are essential to mediate communication between promoter and enhancer regulatory elements.…”

Section: Discussionmentioning

confidence: 99%

Epigenetic Deregulation of the LMP1/LMP2 Locus of Epstein-Barr Virus by Mutation of a Single CTCF-Cohesin Binding Site

Chen

Martin

Lü

et al. 2014

J Virol

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The chromatin regulatory factors CTCF and cohesin have been implicated in the coordinated control of multiple gene loci in Epstein-Barr virus (EBV) latency. We have found that CTCF and cohesin are highly enriched at the convergent and partially overlapping transcripts for the LMP1 and LMP2A genes, but it is not yet known how CTCF and cohesin may coordinately regulate these transcripts. We now show that genetic disruption of this CTCF binding site (EBV⌬CTCF166) leads to a deregulation of LMP1, LMP2A, and LMP2B transcription in EBV-immortalized B lymphocytes. EBV⌬CTCF166 virus-immortalized primary B lymphocytes showed a decrease in LMP1 and LMP2A mRNA and a corresponding increase in LMP2B mRNA. The reduction of LMP1 and LMP2A correlated with a loss of euchromatic histone modification H3K9ac and a corresponding increase in heterochromatic histone modification H3K9me3 at the LMP2A promoter region in EBV⌬CTCF166. Chromosome conformation capture (3C) revealed that DNA loop formation with the origin of plasmid replication (OriP) enhancer was eliminated in EBV⌬CTCF166. We also observed that the EBV episome copy number was elevated in EBV⌬CTCF166 and that this was not due to increased lytic cycle activity. These findings suggest that a single CTCF binding site controls LMP2A and LMP1 promoter selection, chromatin boundary function, DNA loop formation, and episome copy number control during EBV latency.

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Section: Discussionmentioning

confidence: 99%

Epigenetic Deregulation of the LMP1/LMP2 Locus of Epstein-Barr Virus by Mutation of a Single CTCF-Cohesin Binding Site

Chen

Martin

Lü

et al. 2014

J Virol

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“…WAPAL is a key component of the cohesin complex that regulates the formation of sister chromatids (57). Specifically, replacing WAPAL with soronin from the WAPAL/PDS5 complex leads to sister chromatid cohesion in the S phase (32,33).…”

Section: Figurementioning

confidence: 99%

Allogeneic T cell responses are regulated by a specific miRNA-mRNA network

et al. 2013

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“…Cohesin complex regulates the cohesion and separation of sister chromatids during cell division, and recently has been known to regulate gene transcription associated with cell development and differentiation [78,79]. Cohesion complex is composed by Smc1, Smc3, Rad21 and SA1/2.…”

Section: Cohesin Complex Genesmentioning

confidence: 99%

Gene mutations of acute myeloid leukemia in the genome era

Naoe

Kiyoi

2013

Int J Hematol

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Ten years ago, gene mutations found in acute myeloid leukemia (AML) were conceptually grouped into class I mutation, which causes constitutive activation of intracellular signals that contribute to the growth and survival, and class II mutation, which blocks differentiation and/or enhance self-renewal by altered transcription factors. A cooperative model between two classes of mutations has been suggested by murine experiments and partly supported by epidemiological findings. In the last 5 years, comprehensive genomic analysis proceeded to find new gene mutations, which are found in the epigenome-associated enzymes and the molecules never noticed so far. These new mutations apparently increase the complexity and heterogeneity of AML. Although a long list of gene mutations might have been compiled, the entire picture of molecular pathogenesis in AML remains to be elucidated because gene rearrangement, gene copy number, DNA methylation and expression profiles are not fully studied in conjunction with gene mutations. Comprehensive genome research will deepen the understanding of AML to promote the development of new classification and treatment. This review focuses on gene mutations that were recently discovered by genome sequencing.

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Cohesin ties up the genome

Cited by 24 publications

References 75 publications

Epigenetic Deregulation of the LMP1/LMP2 Locus of Epstein-Barr Virus by Mutation of a Single CTCF-Cohesin Binding Site

Epigenetic Deregulation of the LMP1/LMP2 Locus of Epstein-Barr Virus by Mutation of a Single CTCF-Cohesin Binding Site

Allogeneic T cell responses are regulated by a specific miRNA-mRNA network

Gene mutations of acute myeloid leukemia in the genome era

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