Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

A hominoid-specific signaling axis setting the tempo of synaptic maturation

ABSTRACT: A hominoid-specific signaling axis setting the tempo of synaptic maturation

PROVIDER: PRJNA1031090 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR26468981_1.fastq.gz	Fastqsanger.gz
	SRR26468981_2.fastq.gz	Fastqsanger.gz
	SRR26468982_1.fastq.gz	Fastqsanger.gz
	SRR26468982_2.fastq.gz	Fastqsanger.gz
	SRR26468983_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 10

Similar Datasets

A hominoid-specific signaling axis setting the tempo of synaptic maturation II

Project description:A hominoid-specific signaling axis setting the tempo of synaptic maturation II

| PRJNA1095456 | ENA

A hominoid-specific signaling axis setting the tempo of synaptic maturation

Project description:Compared to that of other mammals, human cortical neurons exhibit higher dendritic complexity and synaptic density, and the maturation process is much protracted. However, the molecular mechanism governing these specific features is unclear. Here, we report that the hominoid-specific gene TBC1D3, a core duplicon in the human genome, promotes dendritic arborization and maintains the slow pace of synaptogenesis. Furthermore, to gain insights into the mechanism by which the TBC1D3-MICAL1-ATRX complex determines the slow pace of spinogenesis, we conducted chromatin immunoprecipitation sequencing (ChIP-seq) experiment using an ATRX antibody targeting the C-terminal region in cultured mouse cortical neurons.

2024-03-31 | GSE246002 | GEO

A hominoid-specific signaling axis setting the tempo of synaptic maturation II

2024-04-10 | GSE263014 | GEO

Head-to-head comparison of targeted transcriptome methods: HTG vs TempO-Seq

Project description:In this work this HTG Edgeseq targeted RNA-seq technology is compared with another analogous approach (TempO-Seq) in order to establish its suitability in a research molecular oncology setting. Comparison was proposed at different levels of biomarkers ranging from single mRNA to more complexes including ten to thousands of genes.

2025-11-25 | GSE300263 | GEO

The dynamic reprogramming of H3K9me3 at hominoid-specific retrotransposons during early human development

Project description:Reprogramming of H3K9me3-dependent heterochromatin is required for early development. How H3K9me3 is involved in early human development is, however, largely unclear. Here, we resolve the temporal landscape of H3K9me3 during human preimplantation development and its regulation for diverse hominoid-specific retrotransposons. At the 8-cell stage, H3K9me3 reprogramming at hominoid-specific retrotransposons termed SINE-VNTR-Alu (SVA) facilitates interaction between certain promoters and SVA-derived enhancers, facilitating the zygotic genome activation. In trophectoderm, de novo H3K9me3 domains prohibit pluripotent transcription factors from binding on hominoid-specific retrotransposons-derived regulatory elements for inner cell mass (ICM)-specific genes. H3K9me3 re-establishment at SVA elements in ICM is associated with higher transcription of DNA damage repair genes, compared to naïve human pluripotent stem cells. Our data demonstrate that species-specific reorganization of H3K9me3-dependent heterochromatin at hominoid-specific retrotransposons plays important roles during early human development, shedding light on how the epigenetic regulatory network for early development has evolved in mammals.

2022-07-14 | GSE176016 | GEO

Effect of DRP1 mutations on synaptic development during iPSC-derived cortical neuron maturation

Project description:With the advent of exome sequencing, a growing number of children are being identified with de novo loss of function mutations in the large GTPase essential for mitochondrial fission - Dynamin Related Protein 1 (DRP1); these mutations result in severe neurodevelopmental phenotypes such as developmental delay, optic atrophy, and epileptic encephalopathies. Though it is established that mitochondrial fission is an essential precursor to the rapidly changing metabolic needs of the developing cortex, it is not understood how identified mutations in different domains of DRP1 uniquely disrupt cortical development and synaptic maturation. We leveraged the power of both high-resolution imaging and induced pluripotent stem cells (iPSCs) harboring DRP1 mutations in either the GTPase or stalk domains to model early stages of cortical development. Transcriptional profiling of mutant DRP1 cortical neurons during maturation, as well as imaging of organelle dynamics and neuronal synapses, strongly suggests that altered mitochondrial morphology of DRP1 mutant neurons affect synaptic development leading to pathogenic dysregulation of synaptic activity.

2025-06-30 | GSE296512 | GEO

Monozygotic twins discordant for schizophrenia differ in maturation and synaptic transmission

Project description:Monozygotic twins discordant for schizophrenia differ in maturation and synaptic transmission

| PRJNA1098725 | ENA

TempO-Seq sequencing of Dimethylamine

Project description:TempO-Seq sequencing of Dimethylamine

| PRJNA1008258 | ENA

Hominoid-specific transposable elements reshaped neural crest migration in craniofacial development

Project description:Craniofacial development is evolutionarily conserved, yet subtle changes in its regulatory network drive species-specific traits. Transposable elements (TEs) contribute to genome evolution, but their role in cranial neural crest cells (CNCCs) remains unclear. Here, we investigate the domestication of hominoid-specific TEs (LTR5Hs and SVAs) as enhancers during human CNCC specification, a process critical for vertebrate craniofacial development. Using human iPSC-derived CNCCs, we identified ~515 hominoid-specific TEs functioning as enhancers, including ~250 human-specific, predominantly LTR5Hs. These elements are enriched for CNCC coordinator motifs, are bound by the CNCC signature factor TWIST1, and their enhancer activity appears largely CNCC-specific. CRISPR-interference targeting ~75% of these active TEs led to widespread transcriptional dysregulation of genes involved in neural crest migration, and two orthogonal functional assays confirmed that CNCC migration is impaired upon TE repression. Finally, genes near human-specific TEs showed higher expression in human CNCCs compared to chimpanzee CNCCs, but TE repression restored gene expression to chimpanzee levels. These findings highlight how young TEs were domesticated to fine-tune CNCC regulatory networks, potentially contributing to lineage-specific craniofacial evolution.

2025-03-23 | GSE292478 | GEO

Developmental dynamics of the postsynaptic proteome to understand synaptic maturation and dysmaturation

Project description:The postsynaptic density (PSD) is a protein condensate composed of ~1,000 proteins beneath the postsynaptic membrane of excitatory synapses. The number, shape, and plasticity of synapses are altered during development. However, the dynamics of synaptic protein composition across development have not been fully understood. Here we show alterations of PSD protein composition in mouse and primate brains during development. Proteins involved in synapse regulation are enriched in the differentially expressed (288 decreased and 267 increased) proteins on mouse PSD after a 2-week-old, which may be involved in changes of synaptic signal transduction. We find that the changes in PSD protein abundance in mouse brains correlate with gene expression levels in postnatal mice and perinatal primates. Proteome analysis of PSD from developing common marmosets (Callithrix jacchus) shows that the changes of PSD composition in mouse brain after 2-week-old occur in the marmoset brain mainly during the neonatal period and continue until adulthood. We also describe the changes of PSD proteome at the late developmental stage of marmoset, which may be involved in synaptic pruning observed in primate brains. The maturation of PSD composition is likely defective in autism spectrum disorder (ASD). Our results provide a comprehensive architecture of the remodeling of PSD composition across development, which may explain the molecular basics of synapse maturation and the pathology of psychiatric disorders, such as ASD.

2024-01-17 | PXD048549 | Pride

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data