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RAI1 Regulates Activity-Dependent Nascent Transcription and Synaptic Scaling
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Academic Article
research paper
schema:ScholarlyArticle
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Academic Article
research paper
schema:ScholarlyArticle
isDefinedBy
Covid-on-the-Web dataset
has title
RAI1 Regulates Activity-Dependent Nascent Transcription and Synaptic Scaling
Creator
Jones, Kevin
Althaus, J
Carlos, Jean
Chen, Alex
Díaz, Rodríguez
Garay, Patricia
Giger, Roman
Iwase, Shigeki
Kohen, Rafi
Sutton, Michael
Tsukahara, Takao
Wallner, Margarete
Source
PMC
abstract
Long-lasting forms of synaptic plasticity such as synaptic scaling are critically dependent on transcription. Activity-dependent transcriptional dynamics in neurons, however, remain incompletely characterized because most previous efforts relied on measurement of steady-state mRNAs. Here, we use nascent RNA sequencing to profile transcriptional dynamics of primary neuron cultures undergoing network activity shifts. We find pervasive transcriptional changes, in which ∼45% of expressed genes respond to network activity shifts. We further link retinoic acid-induced 1 (RAI1), the Smith-Magenis syndrome gene, to the transcriptional program driven by reduced network activity. Remarkable agreement among nascent transcriptomes, dynamic chromatin occupancy of RAI1, and electrophysiological properties of Rai1-deficient neurons demonstrates the essential roles of RAI1 in suppressing synaptic upscaling in the naive network, while promoting upscaling triggered by activity silencing. These results highlight the utility of bona fide transcription profiling to discover mechanisms of activity-dependent chromatin remodeling that underlie normal and pathological synaptic plasticity.
has issue date
2020-08-11
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bibo:doi
10.1016/j.celrep.2020.108002
has license
no-cc
sha1sum (hex)
e07a68e06cf2c33ce5f58c9a0af10e3edd8e906e
schema:url
https://doi.org/10.1016/j.celrep.2020.108002
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RAI1 Regulates Activity-Dependent Nascent Transcription and Synaptic Scaling
has PubMed Central identifier
PMC7418709
schema:publication
Cell Rep
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covid:e07a68e06cf2c33ce5f58c9a0af10e3edd8e906e#body_text
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named entity 'protein'
named entity 'ABSTRACT'
covid:arg/e07a68e06cf2c33ce5f58c9a0af10e3edd8e906e
named entity 'naive'
named entity 'RAI1'
named entity 'Graphical'
named entity 'chromatin'
named entity 'transcription'
named entity 'transcription'
named entity 'RAI1'
named entity 'RAI1'
named entity 'Natick'
named entity 'chromatin'
named entity 'neurons'
named entity 'gene transcription'
named entity 'Dunnett's test'
named entity 'multiple comparisons'
named entity 'CD11b'
named entity 'synaptic scaling'
named entity 'neurons'
named entity 'BrU'
named entity 'downregulated'
named entity 'Cell Reports'
named entity 'OPEN ACCESS'
named entity 'RAI1'
named entity 'Downregulation'
named entity 'gene'
named entity 'RAI1'
named entity 'chromatin'
named entity 'mRNA'
named entity 'learning deficits'
named entity 'chromatin'
named entity 'cognitive development'
named entity 'EHMT1'
named entity 'RAI1'
named entity 'chromatin'
named entity 'cell types'
named entity 'San Diego'
named entity 'excitatory postsynaptic currents'
named entity 'TET3'
named entity 'neuronal network'
named entity 'Smith-Magenis syndrome'
named entity 'BrU'
named entity 'statistical significance'
named entity 'August 11'
named entity 'RAI1'
named entity 'synaptic strength'
named entity 'hippocampal'
named entity 'synaptic scaling'
named entity 'cumulative probability distributions'
named entity 'hippocampal'
named entity 'astrocytes'
named entity 'RAI1'
named entity 'E18'
named entity 'D-lysine'
named entity 'antibody'
named entity 'bimodal distribution'
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named entity 'RNAs'
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named entity 'cognitive deficits'
named entity 'heterozygous'
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named entity 'forebrain'
named entity 'neurons'
named entity 'correlation'
named entity 'transfection'
named entity 'inhibitory neurons'
named entity 'Olig2'
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