Gene expression data from activity dependent genes in post mitotic-neurons
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PROVIDER: PRJNA686977 | ENA |
REPOSITORIES: ENA
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Project description:Neurons express numerous genes in response to environmental stimuli. This activity-dependent transcription is vital for neurons to function and hence for the brain to exert its complex processes. Post translational modifications of core histones have been implicated in the regulation of neuronal activity-dependent transcription. On the other hand, transcription and repair also involves the exchange of core histones, which regulates histone metabolism, but its involvement in neural activity-dependent transcription is currently well unknown. Here, in mature postmitotic neurons derived from mouse hippocampus, a Hist1h3f gene, which encodes replication-dependent histone H3.2, is expressed upon stimulation to glutamine receptors. Salt extraction and metabolic labeling of newly synthesized proteins in neurons revealed that core histone proteins are increased at protein levels in response to glutamine receptor stimulation. These results suggest that newly synthesized replication-dependent histone play a role in post-mitotic neurons. We performed microarrays to investigte the global transcriptional profiles of activity-dependent gene expression and identified two class of up-regulated genes during this process.
2020-12-22 | GSE163636 | GEO
Project description:Once generated, neurons are thought to permanently exit the cell cycle and become irreversibly differentiated. However, neither the precise point at which this post-mitotic state is attained nor the extent of its irreversibility is clearly defined. Here we report that newly born neurons from the upper layers of the mouse cortex, despite initiating axon and dendrite elongation, continue to drive gene expression from the neurogenic intermediate neural progenitor tubulin ?1 promoter (T?1p). These observations suggest an ambiguous post-mitotic neuronal state. Whole transcriptome analysis of sorted upper cortical neurons further revealed that neurons continue to express genes related to cell cycle progression long after mitotic exit until at least post-natal day 3 (P3). These genes are however down regulated thereafter and are associated with a concomitant up regulation of tumor suppressors at P5. Interestingly, newly born neurons located in the cortical plate (CP) at embryonic day 18-19 (E18-E19) and P3 challenged with calcium influx are found in S/G2/M phases of the cell cycle, and still able to undergo division at E18-E19 but not at P3. At P5 however, calcium influx becomes neurotoxic and leads instead to neuronal loss. Our data delineate for the first time the temporal window during which developing neurons acquire a post-mitotic state.
2014-09-29 | GSE61845 | GEO
Project description:Activity-dependent transcriptional changes in human neurons
| PRJNA313218 | ENA
Project description:In order to gain a greater understanding of the role of the condensin subunit Cap-G in post-mitotic neurons, we profiled the binding of Cap-G to chromatin in neurons (at different stages of maturation) and neural stem cells in Drosophila using Targeted DamID. We also performed RNA-seq on larval brains that had Cap-G was knocked-down specifically in neurons.
2019-12-17 | GSE142112 | GEO
Project description:Temporal transitions in post-mitotic neurons throughout the C. elegans nervous system
| PRJNA664707 | ENA
Project description:The nervous system of animals is functional at early postembryonic stages but undergoes extensive anatomical and functional changes throughout postembryonic development to eventually form a fully mature nervous system at adulthood. The molecular changes in post-mitotic neurons across post-embryonic development and the genetic programs that control these temporal transitions are not well understood. Using the model organism C. elegans, we comprehensively characterized the distinct functional states (locomotor behavior) and corresponding distinct molecular states (transcriptome) of the post-mitotic nervous system across temporal transitions from early post-embryonic periods to adulthood. We observed pervasive changes in gene expression, many of which controlled by the conserved heterochronic miRNA lin-4/mir-125 and its target, the transcription factor lin-14. The functional relevance of these molecular, lin-4/lin-14 controlled transitions are exemplified by a novel neuropeptide, nlp-45, which confers temporally controlled anti-exploratory activities. Our studies provide new insights into a perhaps generalizable regulatory mechanism that alters neuron-type specific gene batteries to modulate distinct behaviors states, and also provides a rich atlas of post-embryonic molecular changes to uncover additional regulatory mechanisms.
2021-10-25 | GSE158274 | GEO
Project description:The nervous system of animals is functional at early postembryonic stages but undergoes extensive anatomical and functional changes throughout postembryonic development to eventually form a fully mature nervous system at adulthood. The molecular changes in post-mitotic neurons across post-embryonic development and the genetic programs that control these temporal transitions are not well understood. Using the model organism C. elegans, we comprehensively characterized the distinct functional states (locomotor behavior) and corresponding distinct molecular states (transcriptome) of the post-mitotic nervous system across temporal transitions from early post-embryonic periods to adulthood. We observed pervasive changes in gene expression, many of which controlled by the conserved heterochronic miRNA lin-4/mir-125 and its target, the transcription factor lin-14. The functional relevance of these molecular, lin-4/lin-14 controlled transitions are exemplified by a novel neuropeptide, nlp-45, which confers temporally controlled anti-exploratory activities. Our studies provide new insights into a perhaps generalizable regulatory mechanism that alters neuron-type specific gene batteries to modulate distinct behaviors states, and also provides a rich atlas of post-embryonic molecular changes to uncover additional regulatory mechanisms.
2021-10-25 | GSE181288 | GEO
Project description:Characterisation of Cap-G binding and its role in post-mitotic neurons in Drosophila
| PRJNA595925 | ENA
Project description:Temporal transitions in post-mitotic neurons throughout the C. elegans nervous system [ChIP-seq]
| PRJNA751424 | ENA
Project description:ATRX is a member of the SWI2/SNF2 family of chromatin remodeling proteins and primarily functions at heterochromatic loci via its recognition of M-bM-^@M-^XrepressiveM-bM-^@M-^Y histone modifications (e.g., H3K9me3). Despite significant roles for ATRX during normal neural development, as well as its relationship to human disease, ATRX function in the central nervous system is not well understood. Here, we describe ATRXM-bM-^@M-^Ys ability to recognize an activity-dependent combinatorial histone modification, H3K9me3S10ph, in post-mitotic neurons. In neurons, this M-bM-^@M-^\methyl/phosM-bM-^@M-^] switch occurs exclusively following periods of stimulation and is highly enriched at heterochromatic repeats associated with centromeres. Using a multifaceted approach, we reveal that H3K9me3S10ph bound Atrx represses non-coding transcription of centromeric minor satellite sequences during instances of heightened activity. Our results indicate an essential interaction between ATRX and a previously uncharacterized histone modification in the central nervous system and suggest a potential role for abnormal repetitive element transcription in pathological states manifested by ATRX dysfunction. For Atrx ChIP-seq, IPs were performed on three control vs. three KCl stimulated (all representing biological, and not technical replicates) primary cultured mouse cortical neurons at DIV 8. All samples were normalized to background input levels. For H3K9me3S10phos ChIP-seq, biological singlecates (control vs. forskolin) were analyzed against respective inputs.
2015-01-02 | E-GEOD-64062 | biostudies-arrayexpress