Interaction of the Repressor Element 1-silencing Transcription Factor (REST) with Target Genes

Wood, Ian C.; Belyaev, Nikolai D.; Bruce, Alexander W.; Jones, Coleen; Mistry, Mohini; Roopra, Avtar; Buckley, Noel J.

doi:10.1016/j.jmb.2003.10.017

Cited by 51 publications

(95 citation statements)

References 41 publications

(49 reference statements)

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“…Sequences encoding the DNA binding domain of REST/NRSF (amino acid residues 234 -437) fused to a myc epitope were excised from pMTDomNeg12 and inserted into pAdTrack-CMV (Wood et al, 2003). Plaque-forming virus particles (109 U/ml) were used to infect Hdh 7/7 and Hdh 109/109 cells.…”

Section: Methodsmentioning

confidence: 99%

“…Plaque-forming virus particles (109 U/ml) were used to infect Hdh 7/7 and Hdh 109/109 cells. RNA and proteins were harvested 48 h later as described in Wood et al (2003). The same assay was performed with similar results by transfecting cells with Lipofectamine PLUS (Invitrogen) according to manufacturer's instructions.…”

Section: Methodsmentioning

confidence: 99%

“…We have previously shown that many REST/NRSF targets that are silent in non-neural cells are inaccessible to REST/NRSF (Wood et al, 2003;Belyaev et al, 2004). Accordingly, we postulated that such targets would be refractory to increases in nuclear REST/NRSF consequent to expression of mutant huntingtin, thus conferring brain specificity to the dysfunction of the REST/NRSF-NRSE signaling pathway.…”

Section: Rest/nrsf Binding At the Endogenous Re1/nrse In Hd Cells Andmentioning

confidence: 99%

“…Accordingly, we used a dominant-negative REST/NRSF construct (DN:REST) comprising the DNA binding domain (Wood et al, 2003;Belyaev et al, 2004;Bruce et al, 2004) to attenuate REST/NRSF binding to its cognate RE1/NRSE sites in Hdh 109/109 mutant huntingtin knock-in cells. These experiments showed that 48 h after delivery of DN:REST into Hdh 109/109 cells, Bdnf mRNA was increased to similar levels to that seen in untreated wild-type Hdh 7/7 cells (Fig.…”

Section: Expression Of Dominant-negative Rest/nrsf Derepresses Neuronmentioning

confidence: 99%

“…RE1 silencing transcription factor/neuron-restrictive silencer factor (REST/NRSF) is a transcription factor (Chong et al,1995;Schoenherr and Anderson, 1995) that is recruited to RE1/NRSE sites, repressing or silencing neuron-specific genes in both neural (Palm et al, 1998(Palm et al, , 1999Wood et al, 2003) and non-neural (Belyaev et al, 2004) cells. We reported that wildtype huntingtin sequesters REST/NRSF in the cytoplasm, thereby permitting activated transcription of the BDNF gene.…”

Section: Introductionmentioning

confidence: 99%

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Widespread Disruption of Repressor Element-1 Silencing Transcription Factor/Neuron-Restrictive Silencer Factor Occupancy at Its Target Genes in Huntington's Disease

Zuccato¹,

Belyaev²,

Conforti³

et al. 2007

Journal of Neuroscience

244

245

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Huntingtin is a protein that is mutated in Huntington's disease (HD), a dominant inherited neurodegenerative disorder. We previously proposed that, in addition to the gained toxic activity of the mutant protein, selective molecular dysfunctions in HD may represent the consequences of the loss of wild-type protein activity. We first reported that wild-type huntingtin positively affects the transcription of the brain-derived neurotrophic factor (

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Rest/nrsf Binding At the Endogenous Re1/nrse In Hd Cells Andmentioning

confidence: 99%

Section: Expression Of Dominant-negative Rest/nrsf Derepresses Neuronmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Widespread Disruption of Repressor Element-1 Silencing Transcription Factor/Neuron-Restrictive Silencer Factor Occupancy at Its Target Genes in Huntington's Disease

Zuccato¹,

Belyaev²,

Conforti³

et al. 2007

Journal of Neuroscience

244

245

View full text Add to dashboard Cite

show abstract

Mouse and rat BDNF gene structure and expression revisited

Aid¹,

Kazantseva²,

Piirsoo³

et al. 2006

J of Neuroscience Research

858

898

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Brain-derived neurotrophic factor (BDNF) has important functions in the development of the nervous system and in brain plasticity-related processes such as memory, learning, and drug addiction. Despite the fact that the function and regulation of rodent BDNF gene expression have received close attention during the last decade, knowledge of the structural organization of mouse and rat BDNF gene has remained incomplete. We have identified and characterized several mouse and rat BDNF transcripts containing novel 5 0 untranslated exons and introduced a new numbering system for mouse and rat BDNF exons. According to our results both mouse and rat BDNF gene consist of eight 5 0 untranslated exons and one protein coding 3 0 exon. Transcription of the gene results in BDNF transcripts containing one of the eight 5 0 exons spliced to the protein coding exon and in a transcript containing only 5 0 extended protein coding exon. We also report the distinct tissue-specific expression profiles of each of the mouse and rat 5 0 exon-specific transcripts in different brain regions and nonneural tissues. In addition, we show that kainic acid-induced seizures that lead to changes in cellular Ca 2+ levels as well as inhibition of DNA methylation and histone deacetylation contribute to the differential regulation of the expression of BDNF transcripts. Finally, we confirm that mouse and rat BDNF gene loci do not encode antisense mRNA transcripts, suggesting that mechanisms of regulation for rodent and human BDNF genes differ substantially. V V C 2006 Wiley-Liss, Inc.

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RE1 silencing transcription factor/neuron‐restrictive silencing factor regulates expansion of adult mouse subventricular zone‐derived neural stem/progenitor cells in vitro

Soldati

Caramanica

Burney

et al. 2015

J of Neuroscience Research

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Adult neural stem cell (aNSC) activity is tuned by external stimuli through the recruitment of transcription factors. This study examines the RE1 silencing transcription factor (REST) in neural stem/progenitor cells isolated from the subventricular zone of adult mouse brain and provides the first extensive characterization of REST-mediated control of the cellular and molecular properties. This study shows that REST knockdown affects the capacity of progenitor cells to generate neurospheres, reduces cell proliferation, and triggers cell differentiation despite the presence of growth factors. Genome- and transcriptome-wide analyses show that REST binding sites are significantly enriched in genes associated with synaptic transmission and nervous system development and function. Seeking candidate regulators of aNSC function, this study identifies a member of the bone morphogenetic protein (BMP) family, BMP6, the mRNA and protein of which increased after REST knockdown. The results of this study extend previous findings, demonstrating a reciprocal control of REST expression by BMPs. Administration of exogenous BMP6 inhibits aNSC proliferation and induces the expression of the astrocytic marker glial fibrillary acidic protein, highlighting its antimitogenic and prodifferentiative effects. This study suggests that BMP6 produced in a REST-regulated manner together with other signals can contribute to regulation of NSC maintenance and fate.

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Interaction of the Repressor Element 1-silencing Transcription Factor (REST) with Target Genes

Cited by 51 publications

References 41 publications

Widespread Disruption of Repressor Element-1 Silencing Transcription Factor/Neuron-Restrictive Silencer Factor Occupancy at Its Target Genes in Huntington's Disease

Widespread Disruption of Repressor Element-1 Silencing Transcription Factor/Neuron-Restrictive Silencer Factor Occupancy at Its Target Genes in Huntington's Disease

Mouse and rat BDNF gene structure and expression revisited

RE1 silencing transcription factor/neuron‐restrictive silencing factor regulates expansion of adult mouse subventricular zone‐derived neural stem/progenitor cells in vitro

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