Neural restrictive silencer factor recruits mSin3 and histone deacetylase complex to repress neuron-specific target genes

Naruse, Yoshihisa; Aoki, Tsutomu; Kojima, Takao; Mori, Nozomu

doi:10.1073/pnas.96.24.13691

Cited by 219 publications

(198 citation statements)

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“…REST binds the RE1 element of target genes and recruits CoREST (Andres et al, 1999;Ballas et al, 2001) and mSin3A (Naruse et al, 1999;Huang et al, 1999;Grimes et al, 2000;Roopra et al, 2001), corepressor platforms which in turn recruit HDACs-1 and 2. HDACs deacetylate core histone proteins and affect dynamic and reversible gene silencing (Roopra et al, 2001;Ooi and Wood, 2007).…”

Section: Transcriptional Regulation By Rest During Strokementioning

confidence: 99%

Epigenetic Mechanisms in Stroke and Epilepsy

Hwang

Aromolaran

Zukin

2012

Neuropsychopharmacol

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Epigenetic remodeling and modifications of chromatin structure by DNA methylation and histone modifications represent central mechanisms for the regulation of neuronal gene expression during brain development, higher-order processing, and memory formation. Emerging evidence implicates epigenetic modifications not only in normal brain function, but also in neuropsychiatric disorders. This review focuses on recent findings that disruption of chromatin modifications have a major role in the neurodegeneration associated with ischemic stroke and epilepsy. Although these disorders differ in their underlying causes and pathophysiology, they share a common feature, in that each disorder activates the gene silencing transcription factor REST (repressor element 1 silencing transcription factor), which orchestrates epigenetic remodeling of a subset of 'transcriptionally responsive targets' implicated in neuronal death. Although ischemic insults activate REST in selectively vulnerable neurons in the hippocampal CA1, seizures activate REST in CA3 neurons destined to die. Profiling the array of genes that are epigenetically dysregulated in response to neuronal insults is likely to advance our understanding of the mechanisms underlying the pathophysiology of these disorders and may lead to the identification of novel therapeutic strategies for the amelioration of these serious human conditions.

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Section: Transcriptional Regulation By Rest During Strokementioning

confidence: 99%

Epigenetic Mechanisms in Stroke and Epilepsy

Hwang

Aromolaran

Zukin

2012

Neuropsychopharmacol

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“…The demethylating agents such as 5-aza-2'deoxycytidine (5-aza-CdR) and its homologues or valproic acid (VPA) are usually used for studying gene regulation [64] . Researches indicate that TSA can alleviate the transcription repression of the genes containing NRSE [61] . Hsieh et al [25] found that adult multipotent neural progenitor cells predominantly differentiated into neurons but not glia since glial differentiation was actively suppressed in the presence of VPA (Fig.2B).…”

Section: The Structure Of Mirna Researches Indicate That Mirnas Are Pmentioning

confidence: 99%

“…NRSE/NRSF can mediate transcriptional repression through associating with the mSin3A/B complex [61] , N-CoR [62] , and the novel co-repressor complex [55] CoREST/HDAC2 [63] . CoREST can recruit other silencing machinery to NRSF target genes, including the methyl-DNA binding protein MeCP2, heterochromatin protein 1, and histone lysine methyltransferase (the suppressor of variegation 39H1) [59] .…”

Section: Non-coding Rnasmentioning

confidence: 99%

“…There is a cluster of eight zinc finger repeats near its N-terminus, followed by a region rich in basic amino acids, a cluster of six proline-rich repeats, and a single zinc-finger near the C terminus. Su et al showed that the NSCs transfected with recombinant transcriptional factor NRSF-VP16 could directly activate the target genes inhibited by NRSF and efficiently induce NSCs to differentiate into neurons [60] .NRSE/NRSF can mediate transcriptional repression through associating with the mSin3A/B complex [61] , N-CoR [62] , and the novel co-repressor complex [55] CoREST/HDAC2 [63] . CoREST can recruit other silencing machinery to NRSF target genes, including the methyl-DNA binding protein MeCP2, heterochromatin protein 1, and histone lysine methyltransferase (the suppressor of variegation 39H1) [59] .…”

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confidence: 99%

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Epigenetics and neural stem cell commitment

Zhu

2007

Neurosci. Bull.

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Neural stem cell is presently the research hotspot in neuroscience. Recent progress indicates that epigenetic modulation is closely related to the self-renewal and differentiation of neural stem cell. Epigenetics refer to the study of mitotical/meiotical heritage changes in gene function that cannot be explained by changes in the DNA sequence. Major epigenetic mechanisms include DNA methylation, histone modification, chromatin remodeling, genomic imprinting, and non-coding RNA. In this review, we focus on the new insights into the epigenetic mechanism for neural stem cells fate.Key words: stem cells; epigenesis; neuron restrictive silencer element; genomic imprinting; H19; non-coding RNA Epigenetics, a newly arising subject in genetics, refers to the heritable changes of gene function that would ultimately result in cellular specification transformation without altering the genome sequence. In 1942, Waddington CH firstly raised the term "epigenetics", pointing out that it was related to genetics and mainly dealt with the links between genetic identity and epigenetic identity. Later, Holiday R drew more systemic conclusion that the objective of epigenetics was to study the heritable pattern of gene expression change without DNA sequence alteration [1] . The epigenetic mechanisms cover a wide range, containing DNA methylation, histone modification (such as acetylation), chromatin remodeling, genomic imprinting, and regulatory non-coding RNAs. These epigenetic factors are closely related to regulate gene expression (Fig. 1). Recently, more and more investigations have shown that epigenetic modifications play important roles in neural stem cell (NSC) commitment [2,3] , which would be discussed in this review. DNA methylationOne class of epigenetic modifications is DNA cytosine methylation, which consistently associated with diverse gene regulatory processes, for instance, genomic imprinting [4] . In vertebrates, DNA methylation mainly takes place at CpG dinucleotides. Clusters of CpG dimer known as CpG islands are located on the region of gene promoter. During the process of DNA methylation, cytosine is out of DNA double helix and enters the split that binds to the cytosine methyltransferase. The latter transfers the methyl of sadenosylmethionine (SAM) to the 5' of cytosine, forming 5-methyl-cytosine. DNA methylation is carried out by the DNA methyl transferase (DNMT) protein family, which is split into three kinds in mammals: DNMT1, DNMT2 and DNMT3. DNMT3a and DNMT3b [5] was originally described as de novo methyltransferases; DNMT1 could maintain methylation; and DNMT2 was found as a homologue to the Schizosac-charomyces pombe DNA methyltransferase.DNA methylation-mediated gene silencing is regulated through two mechanisms: 1, the methylation at CpG sites blocks transcription factor binding and leads to transcriptional inactivation; and 2, methyl-CpGs are bound by a family of methyl-CpG binding proteins (MBDs), including MBD1-4 and MeCP2. The MBDs binding and the further recruitment of histone deacety...

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“…REST is a powerful repressor. The N terminus of the molecule has the ability to recruit HDAC1/2 complexes and Sin3A, whereas its C terminus has the ability to form complexes with HDAC1/2 and with Co-REST (Andres et al 1999;Huang et al 1999;Naruse et al 1999;Roopra et al 2000). Accordingly, neuronal differentiation of embryonic or adult neural progenitors is initiated by the removal component of these large repressive complexes.…”

Section: Modulation Of Oligodendrocyte Lineage-specific Pathways By Hmentioning

confidence: 99%

Post-Translational Modifications of Nucleosomal Histones in Oligodendrocyte Lineage Cells in Development and Disease

Shen

Casaccia‐Bonnefil

2007

J Mol Neurosci

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The role of epigenetics in modulating gene expression in the development of organs and tissues and in disease states is becoming increasingly evident. Epigenetics refers to the several mechanisms modulating inheritable changes in gene expression that are independent of modifications of the primary DNA sequence and include post-translational modifications of nucleosomal histones, changes in DNA methylation, and the role of microRNA. This review focuses on the epigenetic regulation of gene expression in oligodendroglial lineage cells. The biological effects that posttranslational modifications of critical residues in the N-terminal tails of nucleosomal histones have on oligodendroglial cells are reviewed, and the implications for disease and repair are critically discussed.

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Neural restrictive silencer factor recruits mSin3 and histone deacetylase complex to repress neuron-specific target genes

Cited by 219 publications

References 61 publications

Epigenetic Mechanisms in Stroke and Epilepsy

Epigenetic Mechanisms in Stroke and Epilepsy

Epigenetics and neural stem cell commitment

Post-Translational Modifications of Nucleosomal Histones in Oligodendrocyte Lineage Cells in Development and Disease

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