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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE263014 | GEO | 2024/04/10

REPOSITORIES: GEO

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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

Mitochondria Metabolism Sets the Species-Specific Tempo of Neuronal Development

Project description:Neuronal development in the human cerebral cortex is considerably prolonged compared to that of other mammals. We explored whether mitochondria influence the species-specific timing of cortical neuron maturation. By comparing human and mouse cortical neuronal maturation at high temporal and cell resolution, we found a slower mitochondria development in human cortical neurons compared with that in the mouse, together with lower mitochondria metabolic activity, particularly that of oxidative phosphorylation. Stimulation of mitochondria metabolism in human neurons resulted in accelerated development in vitro and in vivo, leading to maturation of cells weeks ahead of time, whereas its inhibition in mouse neurons led to decreased rates of maturation. Mitochondria are thus important regulators of the pace of neuronal development underlying human-specific brain neoteny.

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

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

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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

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TBC1D3 Associates with the Histone Lysine N-methyltransferase G9a to Affect the Promotion of Neural Progenitors and Cortical Expansion in an Epigenetic Way [ChIP-Seq]

Project description:we conducted chromotin Immunoprecipitation sequencing (ChIP-seq) using mouse cortical tissues from TBC1D3-transgenic mice and wild-typed mice

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Bulk RNA sequencing from sorted VChIs

Project description:VIP/ChAT colinergic interneurons were isolated from mouse cortices with the NuNeX Method described in the manuscript. Cortical neuronal networks control cognitive output, but their composition and modulation remain elusive. Here, we studied the morphological and transcriptional diversity of cortical cholinergic VIP/ChAT interneurons (VChIs), a sparse population with a largely unknown function. We focused on VChIs from the whole barrel cortex and developed a high-throughput automated reconstruction framework, termed PopRec, to characterize hundreds of VChIs from each mouse in an unbiased manner, while preserving 3D cortical coordinates in multiple cleared mouse brains, accumulating thousands of cells. We identified two fundamentally distinct morphological types of VChIs, bipolar and multipolar that differ in their cortical distribution and general morphological features. Following mild unilateral whisker deprivation on postnatal day seven, we found after three weeks both ipsi- and contralateral dendritic arborization differences and modified cortical depth and distribution patterns in the barrel fields alone. To seek the transcriptomic drivers, we developed NuNeX, a method for isolating nuclei from fixed tissues, to explore sorted VChIs. This highlighted differentially expressed neuronal structural transcripts, altered exitatory innervation pathways and established Elmo1 as a key regulator of morphology following deprivation.

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ATRX tolerates activity-dependent histone H3 M-bM-^@M-^\methyl/phos switchingM-bM-^@M-^] to maintain repetitive element silencing in neurons

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.

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Project description:DNA methylation is a major epigenetic factor regulating genome reprogramming, cell differentiation, developmental gene expression. To understand the role DNA methylation in CNS neurons, we generated conditional Dnmt1 mutant mice that possess ~90% hypomethylated cortical and hippocampal cells in the dorsal forebrain from E13.5 on. The mutant mice were viable with a normal lifespan, but displayed severe neuronal cell death between E14.5 to 3-weeks postnatally. Accompanied with the striking cortical and hippocampal degeneration, adult mutant mice exhibited neurobehavioral defects in learning and memory in adulthood. Unexpectedly, a fraction of Dnmt1-/- cortical neurons survived through postnatal development, so that the residual cortex in mutant mice contained 20-30% of hypomethylated neurons throughout the life. Hypomethylated excitatory neurons exhibited multiple defects in postnatal maturation including abnormal dendritic arborization and impaired neuronal excitability. The mutant phenotypes are coupled with deregulation of those genes involved in neuronal layer-specification, cell death, and the function of ion channels. Our results suggest that DNA methylation, through its role in modulating neuronal gene expression, plays multiple roles in regulating cell survival, neuronal migration and maturation in the CNS. Experiment Overall Design: We compared gene expression patterns in Wildtype and DNA methylation deficient (Emx1-cre; Dnmt1 mutant) mouse dorsal cortex. We performed 3 replicates using different each individual mouse strain. The Sample GSM350992 table is the average log ratio for the 3 replicatesArrays were performed in triplicate.

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