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Temporal inhibition of chromatin looping and enhancer accessibility during neuronal remodeling.

ABSTRACT: Temporal inhibition of chromatin looping and enhancer accessibility during neuronal remodeling.

PROVIDER: PRJNA646944 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12248066.fastq.gz	Fastqsanger.gz
	SRR12248067.fastq.gz	Fastqsanger.gz
	SRR12248068.fastq.gz	Fastqsanger.gz
	SRR12248069.fastq.gz	Fastqsanger.gz
	SRR12248070.fastq.gz	Fastqsanger.gz

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Temporal inhibition of chromatin looping and enhancer accessibility during neuronal remodeling.

Project description:We report the 4C-seq data and ChIP-seq to study Shep regulation of chromatin looping. We also reported ATAC-seq and CUT&Tag data on sorted neurons that reveal chromatin accessibility and states during the neuronal remodeling of Drosophila melanogaster

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Temporal inhibition of chromatin looping and enhancer accessibility during neuronal remodeling.

Project description:During development, looping of an enhancer to a promoter is frequently observed in conjunction with temporal and tissue-specific transcriptional activation. The chromatin insulator-associated protein Alan Shepard (Shep) promotes Drosophila post-mitotic neuronal remodeling by repressing transcription of master developmental regulators, such as brain tumor (brat), specifically in maturing neurons. Since insulator proteins can promote looping, we hypothesized that Shep antagonizes brat promoter interaction with an as yet unidentified enhancer. Using chromatin conformation capture and reporter assays, we identified two enhancer regions that increase in looping frequency with the brat promoter specifically in pupal brains after Shep depletion. The brat promoters and enhancers function independently of Shep, ruling out direct repression of these elements. Moreover, ATAC-seq in isolated neurons demonstrates that Shep restricts chromatin accessibility of a key brat enhancer as well as other enhancers genome-wide in remodeling pupal but not larval neurons. These enhancers are enriched for chromatin targets of Shep and are located at Shep-inhibited genes, suggesting direct Shep inhibition of enhancer accessibility and gene expression during neuronal remodeling. Our results provide evidence for temporal regulation of chromatin looping and enhancer accessibility during neuronal maturation.

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Neuronal chromatin remodeling factors in the mammalian nervous system

Project description:Chromatin remodeling factors play important roles in accessibility formation of regulatory DNA. The mechanism by which chromatin remodeling factors regulate regulatory DNA regions that activate expression of cell type-specific genes during the nervous system development remains unknown. Chromatin remodeling complexes have neuron-specific factors, which are often mutated in patients with neurological disease. Here we demonstrate that neuronal chromatin remodeling factors activate neuronal gene expression during the nervous system development.

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RNA-seq - Combining developmental and perturbation-seq uncovers transcriptional modules orchestrating neuronal remodeling

Project description:Developmental neuronal remodeling is an evolutionarily conserved mechanism required for accurate wiring of mature nervous systems. Despite its fundamental role in neurodevelopment and proposed contribution to various neuropsychiatric disorders, the mechanisms instructing remodeling are only partially known. Here, we uncover the fine temporal transcriptional landscape of a stereotypic remodeling event - that of the Drosophila mushroom body γ neurons. To enrich and complement this developmental expression atlas, we also sequenced developing γ neurons perturbed for three key transcription factors known to regulate pruning. Together, these datasets allowed us to construct the developmental and temporal framework of transcriptional modules that together drive remodeling. Moreover, we identified 10 DNA binding proteins that are involved in various aspects of remodeling, and describe their hierarchical relationships. Overall, this study provides the first broad and detailed molecular insight into the complex regulatory dynamics of developmental neuronal remodeling.

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Project description:Direct neuronal reprogramming by temporal identity factors

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Direct neuronal reprogramming by temporal identity factors

Project description:Temporal identity factors are sufficient to reprogram developmental competence of neural progenitors and shift cell fate output, but whether they can also reprogram the identity of terminally differentiated cells is unknown. To address this question, we designed a conditional gene expression system that allows rapid screening of potential reprogramming factors in mouse retinal glial cells combined with genetic lineage tracing. Using this assay, we found that co-expression of the early temporal identity transcription factors Ikzf1 and Ikzf4 is sufficient to directly convert Müller glial cells into cells that translocate to the outer nuclear layer (ONL), where photoreceptor cells normally reside. We name these “induced ONL (iONL)” cells. Using genetic lineage tracing, histological, immunohistochemical, and single-cell transcriptome and multiome analyses, we show that expression of Ikzf1/4 in Müller glia in vivo, without retinal injury, mostly generate iONL cells that share molecular characteristics with bipolar cells, although a fraction of them stain for Rxrg, a cone photoreceptor marker. Furthermore, we show that co-expression of Ikzf1 and Ikzf4 can reprogram mouse embryonic fibroblasts to induced neurons (iN) in culture by rapidly remodeling chromatin and activating a neuronal gene expression program. This work uncovers general neuronal reprogramming properties for temporal identity factors in terminally differentiated cells.

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Chromatin accessibility profiling of developing cerebellar granule neurons identifies novel neuronal enhancers and reveals a role for Zic transcription factors in neuronal maturation

Project description:To identify chromatin mechanisms of neuronal differentiation, we characterized the relationship between chromatin accessibility and gene expression in cerebellar granule neurons (CGNs) of the developing mouse. We used DNase-seq to globally map accessibility of cis-regulatory elements and RNA-seq to profile transcript abundance at key points in postnatal neuronal differentiation in vivo and in culture. We observed thousands of chromatin accessibility changes as CGNs differentiated and determined that many of these regions function as stage-specific neuronal enhancers. Motif discovery within differentially accessible chromatin regions suggested a novel role for the Zic family of transcription factors in CGN maturation, and we confirmed the association of Zic with these elements by ChIP-seq. Knockdown of Zic1 and Zic2 indicated Zic transcription factors are required to coordinate mature neuronal gene expression patterns. These data reveal chromatin dynamics at thousands of gene regulatory elements that facilitate gene expression patterns necessary for neuronal differentiation and function. Biological triplicate DNase-seq and RNA-seq samples from 3 in vivo cerebellum developmental stages (P7, P14, P60) and 3 cultured CGN stages (isolated granule neuron precursors, +3DIV, and +7DIV) obtained. Zic1 and Zic2 were separately knocked down by lentiviral shRNA in cultured CGNs followed by RNA-seq (2 biological replicates per KD and 2 controls). Zic1/2 ChIP-seq was performed with in vivo cerebellum at two developmental stages (P7 and P60) in duplicate with matching input and IgG controls.

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Reorganization of postmitotic neuronal chromatin accessibility for maturation of serotonergic identity

Project description:Assembly of transcriptomes encoding unique neuronal identities requires selective accessibility of transcription factors to cis-regulatory sequences in nucleosome-embedded postmitotic chromatin. Yet, the mechanisms controlling postmitotic neuronal chromatin accessibility are poorly understood. Here, we show that unique distal enhancers define the Pet1 neuron lineage that generates serotonin (5-HT) neurons. Heterogeneous single cell chromatin landscapes are established early in postmitotic Pet1 neurons and reveal the putative regulatory programs driving Pet1 neuron subtype identities. Distal enhancer accessibility is highly dynamic as Pet1 neurons mature, suggesting the existence of regulatory factors that reorganize postmitotic neuronal chromatin. We find that Pet1 and Lmx1b control chromatin accessibility to select Pet1-lineage specific enhancers for 5-HT neurotransmission. Additionally, these factors are required to maintain chromatin accessibility during early maturation suggesting that postmitotic neuronal open chromatin is unstable and requires continuous regulatory input. Together our findings reveal postmitotic transcription factors that reorganize accessible chromatin for neuron specialization.

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