Primetime for Learning Genes.
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TLDR
It is proposed that bivalent domains are a characteristic feature of the chromatin landscape surrounding their promoters that allows them to be “poised” for rapid response to activate or repress gene expression depending on environmental stimuli.Abstract:
Learning genes in mature neurons are uniquely suited to respond rapidly to specific environmental stimuli. Expression of individual learning genes, therefore, requires regulatory mechanisms that have the flexibility to respond with transcriptional activation or repression to select appropriate physiological and behavioral responses. Among the mechanisms that equip genes to respond adaptively are bivalent domains. These are specific histone modifications localized to gene promoters that are characteristic of both gene activation and repression, and have been studied primarily for developmental genes in embryonic stem cells. In this review, studies of the epigenetic regulation of learning genes in neurons, particularly the brain-derived neurotrophic factor gene (BDNF), by methylation/demethylation and chromatin modifications in the context of learning and memory will be highlighted. Because of the unique function of learning genes in the mature brain, it is proposed that bivalent domains are a characteristic feature of the chromatin landscape surrounding their promoters. This allows them to be “poised” for rapid response to activate or repress gene expression depending on environmental stimuli.read more
Citations
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H3K4/H3K9me3 Bivalent Chromatin Domains Targeted by Lineage-specific DNA Methylation Pauses Adipocyte Differentiation
Yoshihiro Matsumura,Ayano Yoshida,Ryo Nakaki,Yuka Kano,Takeshi Inagaki,Hiroyuki Aburatani,Juro Sakai +6 more
TL;DR: An alternative and previously unknown bivalent modified histone signature in lineage-committed mesenchymal stem cells and preadipocytes that pairs H3K4me3 with H3k9me3 to maintain adipogenic master regulatory genes (Cebpa and Pparg) expressed at low levels yet poised for activation when differentiation is required.
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An Evolutionary Perspective on Why Food Overconsumption Impairs Cognition.
TL;DR: Evidence is discussed suggesting that the reason that overconsumption of energy-rich foods negatively impacts cognition is that signaling pathways that evolved to respond adaptively to food scarcity are relatively disengaged in the setting of continuous food availability.
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Regulation of <scp>AMPAR</scp> trafficking in synaptic plasticity by <scp>BDNF</scp> and the impact of neurodegenerative disease
TL;DR: In this paper , the authors present a review of the role of brain-derived neurotrophic factor (BDNF) signaling in synaptic plasticity and learning and memory in brain disorders such as Alzheimer's.
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Genetics of language and its implications on language interventions.
TL;DR: Medical intervention in terms of epigenetics and neurotransmitter regulation is proposed in addition to effective teaching methods to aid in effective language acquisition.
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Characterization and Transcriptional Activation of the Immediate Early Gene ARC During a Neural Correlate of Classical Conditioning.
TL;DR: This study suggests that the learning-inducible IEG tARC utilizes both paused RNAPII and rapid chromatin modifications that allow for dynamic gene responsiveness required when an organism is presented with a variety of environmental stimuli.
References
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Journal ArticleDOI
A Bivalent Chromatin Structure Marks Key Developmental Genes in Embryonic Stem Cells
Bradley E. Bernstein,Tarjei S. Mikkelsen,Tarjei S. Mikkelsen,Xiaohui Xie,Michael Kamal,Dana J. Huebert,James Cuff,Ben Fry,Alexander Meissner,Marius Wernig,Kathrin Plath,Rudolf Jaenisch,Alexandre Wagschal,Robert Feil,Stuart L. Schreiber,Stuart L. Schreiber,Eric S. Lander,Eric S. Lander +17 more
TL;DR: It is proposed that bivalent domains silence developmental genes in ES cells while keeping them poised for activation, highlighting the importance of DNA sequence in defining the initial epigenetic landscape and suggesting a novel chromatin-based mechanism for maintaining pluripotency.
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Genome-wide maps of chromatin state in pluripotent and lineage-committed cells
Tarjei S. Mikkelsen,Manching Ku,Manching Ku,David B. Jaffe,Biju Issac,Biju Issac,Erez Lieberman Aiden,Erez Lieberman Aiden,Georgia Giannoukos,Pablo Alvarez,William Brockman,Tae Kyung Kim,Richard Koche,Richard Koche,Richard Koche,William Lee,Eric M. Mendenhall,Eric M. Mendenhall,Aisling O'Donovan,Aviva Presser,Carsten Russ,Xiaohui Xie,Alexander Meissner,Marius Wernig,Rudolf Jaenisch,Chad Nusbaum,Eric S. Lander,Eric S. Lander,Bradley E. Bernstein,Bradley E. Bernstein +29 more
TL;DR: The application of single-molecule-based sequencing technology for high-throughput profiling of histone modifications in mammalian cells is reported and it is shown that chromatin state can be read in an allele-specific manner by using single nucleotide polymorphisms.
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Transcriptional repression by the methyl-CpG-binding protein MeCP2 involves a histone deacetylase complex
Xinsheng Nan,Huck-Hui Ng,Colin A. Johnson,Carol D. Laherty,Bryan M. Turner,Robert N. Eisenman,Adrian Bird +6 more
TL;DR: The data suggest that two global mechanisms of gene regulation, DNA methylation and histone deacetylation, can be linked by MeCP2, an abundant nuclear protein that is essential for mouse embryogenesis.
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Methylated DNA and MeCP2 recruit histone deacetylase to repress transcription.
Peter L. Jones,Gert C. Jan Veenstra,Paul A. Wade,Danielle Vermaak,Stefan U. Kass,Nicoletta Landsberger,John Strouboulis,Alan P. Wolffe +7 more
TL;DR: The results establish a direct causal relationship between DNA methylation-dependent transcriptional silencing and the modification of chromatin.
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MeCP2, a key contributor to neurological disease, activates and represses transcription.
Maria H. Chahrour,Sung Yun Jung,Chad A. Shaw,Xiaobo Zhou,Stephen T. C. Wong,Jun Qin,Huda Y. Zoghbi +6 more
TL;DR: It is shown that MeCP2 associates with the transcriptional activator CREB1 at the promoter of an activated target but not a repressed target, and that it can function as both an activator and a repressor of transcription.