Synaptic Activity Causes Minute-scale Changes in BAF Complex Composition and Function [CUT&Run]
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1236400 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR32702182_1.fastq.gz | Fastqsanger.gz | |||
| SRR32702182_2.fastq.gz | Fastqsanger.gz | |||
| SRR32702183_1.fastq.gz | Fastqsanger.gz | |||
| SRR32702183_2.fastq.gz | Fastqsanger.gz | |||
| SRR32702184_1.fastq.gz | Fastqsanger.gz |
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Similar Datasets
Project description:Synaptic Activity Causes Minute-scale Changes in BAF Complex Composition and Function
| PRJNA1027458 | ENA
Project description:Genes encoding subunits of the BAF (mammalian SWI/SNF) ATP-dependent chromatin remodeling complex are among the those most enriched for deleterious de novo mutations in intellectual disabilities and autism spectrum disorder, but the causative molecular pathways are not understood. Synaptic activity in neurons is critical for learning and memory and proper neural development. While BAF is required for activity-dependent developmental processes, such as dendritic outgrowth, the immediate molecular consequences of neuronal activity on BAF complexes are unknown. Here we report that neuronal activity induces dramatic remodeling of the subunit composition of BAF complexes within 15 minutes, concurrent with both phosphorylation and dephosphorylation of its subunits. These biochemical effects are a convergent phenomenon downstream of multiple calcium-activated signaling pathways in neurons and fibroblasts and correspond to changes in BAF-dependent chromatin accessibility. Our studies imply that BAF decodes signals at the membrane by altering the combinatorial composition of its subunits.
2025-03-15 | GSE292056 | GEO
Project description:Genes encoding subunits of the BAF (mammalian SWI/SNF) ATP-dependent chromatin remodeling complex are among the those most enriched for deleterious de novo mutations in intellectual disabilities and autism spectrum disorder, but the causative molecular pathways are not understood. Synaptic activity in neurons is critical for learning and memory and proper neural development. While BAF is required for activity-dependent developmental processes, such as dendritic outgrowth, the immediate molecular consequences of neuronal activity on BAF complexes are unknown. Here we report that neuronal activity induces dramatic remodeling of the subunit composition of BAF complexes within 15 minutes, concurrent with both phosphorylation and dephosphorylation of its subunits. These biochemical effects are a convergent phenomenon downstream of multiple calcium-activated signaling pathways in neurons and fibroblasts and correspond to changes in BAF-dependent chromatin accessibility. Our studies imply that BAF decodes signals at the membrane by altering the combinatorial composition of its subunits.
2025-03-15 | GSE245254 | GEO
Project description:Genes encoding subunits of the BAF (mammalian SWI/SNF) ATP-dependent chromatin remodeling complex are among the those most enriched for deleterious de novo mutations in intellectual disabilities and autism spectrum disorder, but the causative molecular pathways are not understood. Synaptic activity in neurons is critical for learning and memory and proper neural development. While BAF is required for activity-dependent developmental processes, such as dendritic outgrowth, the immediate molecular consequences of neuronal activity on BAF complexes are unknown. Here we report that neuronal activity induces dramatic remodeling of the subunit composition of BAF complexes within 15 minutes, concurrent with both phosphorylation and dephosphorylation of its subunits. These biochemical effects are a convergent phenomenon downstream of multiple calcium-activated signaling pathways in neurons and fibroblasts and correspond to changes in BAF-dependent chromatin accessibility. Our studies imply that BAF decodes signals at the membrane by altering the combinatorial composition of its subunits.
2025-03-15 | GSE245251 | GEO
Project description:Synaptic Activity Causes Minute-scale Changes in BAF Complex Composition and Function [ATAC-Seq]
| PRJNA1027470 | ENA
Project description:Synaptic Activity Causes Minute-scale Changes in BAF Complex Composition and Function [RNA-Seq]
| PRJNA1027473 | ENA
Project description:This SuperSeries is composed of the SubSeries listed below.
2025-03-15 | GSE245256 | GEO
Project description:Loss-of-function mutations in genes coding for subunits of the large, multifarious BRG1/BRM associated factor (BAF) chromatin remodeling complexes are frequently causative for cancer or developmental diseases1-5. Cells lacking the most frequently mutated subunits like the ATPase SMARCA4 typically exhibit drastic chromatin accessibility changes, especially of important regulatory regions6-12. However, so far it remains unknown how these changes are established over time, and whether they are causative for intra-complex synthetic lethalities abrogating the formation (SMARCC1-SMARCC2)8,13,14 or activity (SMARCA4-SMARCA2)15-17 of BAF complexes. Here, we utilize the dTAG system18 to induce acute degradation of BAF subunits in wild-type and BAF mutant backgrounds and analyze the resulting chromatin accessibility changes with high kinetic resolution. We observe that chromatin alterations are established faster than the duration of one cell cycle and that maintaining genome accessibility requires constant ATP-dependent remodeling. Completely abolishing BAF complex function by acute degradation of a synthetic lethal subunit in a paralog-deficient background results in a near-complete loss of chromatin accessibility at BAF-controlled sites, especially at super-enhancers, providing a mechanism for intra-complex synthetic lethalities.
2020-12-23 | PXD018381 | Pride
Project description:Loss-of-function mutations in genes coding for subunits of the large, multifarious BRG1/BRM associated factor (BAF) chromatin remodeling complexes are frequently causative for cancer or developmental diseases. Cells lacking the most frequently mutated subunits, like the ATPase SMARCA4, typically exhibit drastic chromatin accessibility changes, especially of important regulatory regions. However, so far it remains unknown how these changes are established over time, and whether they are causative for intra-complex synthetic lethalities abrogating the formation or activity of BAF complexes. Here, we utilize the dTAG system to induce acute degradation of BAF subunits in wildtype and BAF mutant backgrounds and analyze the resulting chromatin accessibility changes with high kinetic resolution. We observe that chromatin alterations are established faster than the duration of one cell cycle and that maintaining genome accessibility requires constant ATP-dependent remodeling. Completely abolishing BAF complex function by acute degradation of a synthetic lethal subunit in a paralog-deficient background results in a near-complete loss of chromatin accessibility at BAF-controlled sites, especially at super-enhancers, providing a mechanism for intra-complex synthetic lethalities.
2020-12-22 | GSE148175 | GEO
Project description:Recent exon sequencing studies of human tumors have revealed that subunits of mSWI/SNF or BAF complexes are mutated in more than 20% of human malignancies, yet the mechanisms involved in tumor suppression is unclear. BAF chromatin remodeling complexes are polymorphic assemblies that use energy provided by ATP hydrolysis to regulate transcription through the control of chromatin structure and the placement of Polycomb (PcG) across the genome. Several proteins dedicated to this large multi-subunit complex, including SMARCA4 (BRG1) and BAF250A (ARID1A), are mutated at frequencies similar to that of many recognized tumor suppressors. In particular, the core ATPase BRG1 is mutated in 5-10% of childhood medulloblastoma (MB) and greater than 15% of Burkitt's Lymphoma (BL). Here we find a novel function of BAF complexes in decatenating newly replicated sister chromatids, which is necessary for proper chromosome segregation during mitosis. We find that deletion of Brg1, as well as the expression of Brg1 point mutants identified in human tumors leads to anaphase bridge formation (sister chromatids linked by catenated strands of DNA), and a G2/M phase block characteristic of the decatenation checkpoint. Endogenous BAF complexes directly interact with endogenous TopoIIα through BAF250a and are required for TopoIIα binding to about 12,000 sites over the genome. Our results indicate that TopoIIα’s chromatin binding is dependent on the ATPase activity of Brg1, which is compromised in oncogenic Brg1 mutants. These studies indicate that the ability of TopoIIα to prevent DNA entanglement at mitosis requires BAF complexes and suggest that this activity contributes to the role of BAF subunits as tumor suppressors. Examination of sites of TopoIIa activity in WT and Brg1-/- ES cells as defined by TopoIIa-DNA covalent adducts formed in the presence of etoposide
2013-03-30 | E-GEOD-45625 | biostudies-arrayexpress