Temporal transitions in post-mitotic neurons throughout the C. elegans nervous system [ChIP-seq]
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA751424 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR15329100.fastq.gz | Fastqsanger.gz | |||
| SRR15329101.fastq.gz | Fastqsanger.gz | |||
| SRR15329102.fastq.gz | Fastqsanger.gz | |||
| SRR15329103.fastq.gz | Fastqsanger.gz | |||
| SRR15329104.fastq.gz | Fastqsanger.gz |
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Project description:Temporal transitions in post-mitotic neurons throughout the C. elegans nervous system
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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.
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| S-EPMC8785361 | biostudies-literature
Project description:Chromatin compartments reorganize dramatically during cell cycle transitions, shifting from a compartmentalized interphase to a condensed mitotic configuration in which large-scale compartment signals are attenuated. While histone modifications are linked to compartment identity, their contribution to compartment organization remains unclear. Using meiotic (mouse spermatogenesis) and mitotic (mouse neuronal progenitor cell, mNPC) models, we mapped histone landscapes alongside compartment dynamics. We found that histone H4 lysine 16 acetylation (H4K16ac) strongly tracked compartment reorganization, remaining enriched in A compartments during compartmentalization but redistributing upon chromatin compaction. In spermatogenesis, H4K16ac loss on the X chromosome coincided with condensation and H3K9me3 spreading. Machine learning highlighted H4K16ac as a stronger predictor of compartment transitions than H3K27ac. Acute degradation of MOF, the principal H4K16ac acetyltransferase, disrupted both the spatial distribution and global abundance of H4K16ac and progressively impaired compartmentalization in mNPCs. These results position H4K16ac as a histone modification selectively coupled to chromatin compartment transitions.
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Project description:Chromatin compartments reorganize dramatically during cell cycle transitions, shifting from a compartmentalized interphase to a condensed mitotic configuration in which large-scale compartment signals are attenuated. While histone modifications are linked to compartment identity, their contribution to compartment organization remains unclear. Using meiotic (mouse spermatogenesis) and mitotic (mouse neuronal progenitor cell, mNPC) models, we mapped histone landscapes alongside compartment dynamics. We found that histone H4 lysine 16 acetylation (H4K16ac) strongly tracked compartment reorganization, remaining enriched in A compartments during compartmentalization but redistributing upon chromatin compaction. In spermatogenesis, H4K16ac loss on the X chromosome coincided with condensation and H3K9me3 spreading. Machine learning highlighted H4K16ac as a stronger predictor of compartment transitions than H3K27ac. Acute degradation of MOF, the principal H4K16ac acetyltransferase, disrupted both the spatial distribution and global abundance of H4K16ac and progressively impaired compartmentalization in mNPCs. These results position H4K16ac as a histone modification selectively coupled to chromatin compartment transitions.
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Project description:Chromatin compartments reorganize dramatically during cell cycle transitions, shifting from a compartmentalized interphase to a condensed mitotic configuration in which large-scale compartment signals are attenuated. While histone modifications are linked to compartment identity, their contribution to compartment organization remains unclear. Using meiotic (mouse spermatogenesis) and mitotic (mouse neuronal progenitor cell, mNPC) models, we mapped histone landscapes alongside compartment dynamics. We found that histone H4 lysine 16 acetylation (H4K16ac) strongly tracked compartment reorganization, remaining enriched in A compartments during compartmentalization but redistributing upon chromatin compaction. In spermatogenesis, H4K16ac loss on the X chromosome coincided with condensation and H3K9me3 spreading. Machine learning highlighted H4K16ac as a stronger predictor of compartment transitions than H3K27ac. Acute degradation of MOF, the principal H4K16ac acetyltransferase, disrupted both the spatial distribution and global abundance of H4K16ac and progressively impaired compartmentalization in mNPCs. These results position H4K16ac as a histone modification selectively coupled to chromatin compartment transitions.
2026-05-27 | GSE332824 | GEO
Project description:Chromatin compartments reorganize dramatically during cell cycle transitions, shifting from a compartmentalized interphase to a condensed mitotic configuration in which large-scale compartment signals are attenuated. While histone modifications are linked to compartment identity, their contribution to compartment organization remains unclear. Using meiotic (mouse spermatogenesis) and mitotic (mouse neuronal progenitor cell, mNPC) models, we mapped histone landscapes alongside compartment dynamics. We found that histone H4 lysine 16 acetylation (H4K16ac) strongly tracked compartment reorganization, remaining enriched in A compartments during compartmentalization but redistributing upon chromatin compaction. In spermatogenesis, H4K16ac loss on the X chromosome coincided with condensation and H3K9me3 spreading. Machine learning highlighted H4K16ac as a stronger predictor of compartment transitions than H3K27ac. Acute degradation of MOF, the principal H4K16ac acetyltransferase, disrupted both the spatial distribution and global abundance of H4K16ac and progressively impaired compartmentalization in mNPCs. These results position H4K16ac as a histone modification selectively coupled to chromatin compartment transitions.
2026-05-27 | GSE299092 | GEO
Project description:Chromatin compartments reorganize dramatically during cell cycle transitions, shifting from a compartmentalized interphase organization to a condensed mitotic configuration in which large-scale compartment signals are attenuated. While histone modifications are linked to compartment identity, their causal contribution to compartment organization remained unclear. Using meiotic (mouse spermatogenesis) and mitotic (mouse neuronal progenitor cells, mNPCs) models, we mapped histone landscapes alongside compartment dynamics. We found that histone H4 lysine 16 acetylation (H4K16ac) strongly tracked compartment reorganization, remaining enriched in A compartments during compartmentalization but redistributing upon chromatin compaction. In spermatogenesis, H4K16ac loss on the X chromosome coincided with condensation and H3K9me3 spreading. Machine learning highlighted H4K16ac as a stronger predictor of compartment transitions than H3K27ac. To probe causality, we acutely degraded MOF, the principal H4K16ac acetyltransferase, which disrupted both the spatial distribution and global abundance of H4K16ac and progressively impaired compartmentalization in mNPCs. Together, these results position H4K16ac as a selectively coupled and influential histone modification of chromatin compartment transitions.
2026-05-27 | GSE332823 | GEO
Project description:Background: Synaptic transmission is required for functional maturation of the CNS and to induce gene transcription involved in neuronal plasticity. Our aim is to identify genes that are transcriptionally regulated by synaptic transmission during development. cDNA microarrays will be used to compare gene expression in normal embryos and embryos with no synaptic transmission. Using the Gal4 UAS system, the tetanus toxin light fragment (TET) will be expressed throughout the nervous system. The effects of TET are well characterised: the synaptic protein n-Synaptobrevin is cleaved, blocking evokes vesicle fusion in TET expressing neurons and as a result synaptic transmission is blocked. Embryos expressing an inactive, mutant version of TET (iTET) show no detectable phenotype. Thus a comparison of gene expression in iTET expressing embryos and TET expressing embryos focuses our screen cleanly and specifically on genes that are regulated by synaptic transmission. At the end of larval life, during metamorphosis, there is a second phase of nervous system development with the same requirement for neural circuit differentiation and maturation as in the embryo. We will compare gene expression in TET expressing and iTET expressing pupae to identify genes which are regulated by synaptic transmission in this second phase of nervous system development. We will focus our analysis on genes which are similarly regulated in both systems. Plan: elav Gal4 (expressed in all the neurons) for the embryos and Heat Shock Gal4 (which allows a temporally controlled expression) for the pupae are used to drive UAS TET and UAS iTET throughout the nervous system. Crosses are set up with flies homozygous for Gal4 or UAS transgenes, so that all the progeny have the same genotype. Total RNA is extracted from 500 carefully staged embryos that have been collected at the time of hatching. Pupae are heat shocked at 24 hours after puparium formation, and heads are then collected 5 days after puparium formation. TET expressing pupae are paralysed but morphologically normal whereas iTET expressing pupae emerge as normal adults. Total RNA will be extracted from 250 heads of each genotype. Probes made from TET and iTET expressing embryos extracts will be hybridised together to the chip and so will be probes made from TET and iTET expressing pupae extracts. Genes regulated in both systems will be compared together.
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