Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA117989 | ENA |
REPOSITORIES: ENA
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Project description:Mechanism controlling cell fate remains elusive. Chromatin remodeling complex interacts with transcription factors to colocalize across the genome and regulate region-specific epigenetic environment. Here, we propose an engineering approach for controlling cell fate through chromatin closing and opening. We utilize chromatin remodeling complex, BAF, known to activate gene expression by opening chromatin loci. By grafting BAF interacting motifs onto Nanog, we show that engineering factors could promote somatic cell reprogramming with Oct4. Furthermore, mutation on the interacting motifs render iPSC generation. The syntactic factors facilitate cell fate transition by recruiting BAF complex to modulate chromatin accessibility and reorganize cell state specific enhancers. Our findings reveal alternative methods to control cell fate by manipulating chromatin accessibility.
2024-06-24 | GSE263597 | GEO
Project description:Mechanism controlling cell fate remains elusive. Chromatin remodeling complex interacts with transcription factors to colocalize across the genome and regulate region-specific epigenetic environment. Here, we propose an engineering approach for controlling cell fate through chromatin closing and opening. We utilize chromatin remodeling complex, BAF, known to activate gene expression by opening chromatin loci. By grafting BAF interacting motifs onto Nanog, we show that engineering factors could promote somatic cell reprogramming with Oct4. Furthermore, mutation on the interacting motifs render iPSC generation. The syntactic factors facilitate cell fate transition by recruiting BAF complex to modulate chromatin accessibility and reorganize cell state specific enhancers. Our findings reveal alternative methods to control cell fate by manipulating chromatin accessibility.
2024-06-24 | GSE243513 | GEO
Project description:Mechanism controlling cell fate remains elusive. Chromatin remodeling complex interacts with transcription factors to colocalize across the genome and regulate region-specific epigenetic environment. Here, we propose an engineering approach for controlling cell fate through chromatin closing and opening. We utilize chromatin remodeling complex, BAF, known to activate gene expression by opening chromatin loci. By grafting BAF interacting motifs onto Nanog, we show that engineering factors could promote somatic cell reprogramming with Oct4. Furthermore, mutation on the interacting motifs render iPSC generation. The syntactic factors facilitate cell fate transition by recruiting BAF complex to modulate chromatin accessibility and reorganize cell state specific enhancers. Our findings reveal alternative methods to control cell fate by manipulating chromatin accessibility.
2024-06-24 | GSE263598 | GEO
Project description:Mechanism controlling cell fate remains elusive. Chromatin remodeling complex interacts with transcription factors to colocalize across the genome and regulate region-specific epigenetic environment. Here, we propose an engineering approach for controlling cell fate through chromatin closing and opening. We utilize chromatin remodeling complex, BAF, known to activate gene expression by opening chromatin loci. By grafting BAF interacting motifs onto Nanog, we show that engineering factors could promote somatic cell reprogramming with Oct4. Furthermore, mutation on the interacting motifs render iPSC generation. The syntactic factors facilitate cell fate transition by recruiting BAF complex to modulate chromatin accessibility and reorganize cell state specific enhancers. Our findings reveal alternative methods to control cell fate by manipulating chromatin accessibility.
2024-06-24 | GSE243516 | GEO
Project description:Mechanism controlling cell fate remains elusive. Chromatin remodeling complex interacts with transcription factors to colocalize across the genome and regulate region-specific epigenetic environment. Here, we propose an engineering approach for controlling cell fate through chromatin closing and opening. We utilize chromatin remodeling complex, BAF, known to activate gene expression by opening chromatin loci. By grafting BAF interacting motifs onto Nanog, we show that engineering factors could promote somatic cell reprogramming with Oct4. Furthermore, mutation on the interacting motifs render iPSC generation. The syntactic factors facilitate cell fate transition by recruiting BAF complex to modulate chromatin accessibility and reorganize cell state specific enhancers. Our findings reveal alternative methods to control cell fate by manipulating chromatin accessibility.
2024-06-24 | GSE243514 | GEO
Project description:BAF complex is one major group of chromatin remodeling factors in mammals. However, how BAF regulated nucleosomes and other histone modifications is not clear. Here we delete BAF250a, a major component in esBAF to study the nucleosome and histone changes in ESCs. We find that deletion of BAF250a leads to nucleosome occupancy increase in TSS regions and non-pioneer transcription factor binding sites. BAF250a deletion also cause overall decrease of H3K27me3 modification. Collectively, these results reveals how BAF complex coordinates nucleosome, histone modification to control ESC function. Sample 1-4: Nucleosome profiles in WT and BAF250a KO ESCs. Sample 5-10: profiling of H3K4me3 and H3K27me3 in WT and BAF250 KO ESCs.
2015-08-03 | E-GEOD-59082 | biostudies-arrayexpress
Project description:TOP2 synergizes with BAF chromatin remodeling for resolution of facultative heterochromatin
| PRJNA368641 | ENA
Project description:Mutations in the BAF chromatin remodeling complex rank among the most frequent genetic alterations in human cancers, many of which result in a loss of function of the respective subunits. Recent genomic and chemical screens have revealed synthetic lethal interactions of BAF complex subunits with each other as well as with further chromatin modifiers. Using an epigenome-focused shRNA library, we identified loss of the histone chaperone complex CAF-1 (chromatin assembly factor 1) as a synthetic lethal vulnerability of ARID1A-deficient cells that is enhanced by the androgen receptor agonist testosterone. In line with antagonistic roles of the CAF-1 and BAF complexes in nucleosome deposition and remodeling, we show that knock-down of CAF-1 subunits results in a partial reversal of the transcriptional and chromatin accessibility effects caused by loss of ARID1A. Together, our findings identify a new functional partner of the BAF chromatin remodeling complex and represent a potential novel strategy for targeting ARID1A-deficient cancers.
2022-09-01 | GSE125220 | GEO
Project description:Functional crosstalk between histone modifications and chromatin remodeling has emerged as a key regulatory mode of transcriptional control during cell fate decisions, but the underlying mechanisms are not fully understood. Here we demonstrate that HRP2-DPF3a-BAF complex coordinates histone H3 lysine 36 methylation (H3K36me) and ATP-dependent chromatin remodeling to regulate chromatin dynamic and gene transcription during myogenic differentiation. Mechanistically, through its HIV integrase binding domain (IBD), HRP2 associates with BRG1/BRM associated factor (BAF) chromatin remodeling complex by direct interaction with BAF45c (DPF3a) subunit. Through its Pro-Trp-Trp-Pro (PWWP) domain, HRP2 preferentially binds to H3K36me2. Integrative transcriptomic and cistromic analyses, coupled with ATAC-seq, reveal that HRP2 and DPF3a activate myogenic genes by increasing chromatin accessibility through recruitment of BRG1, the ATPase subunit of the BAF complex.
2020-05-13 | GSE148296 | GEO
Project description:Introgressed variants from other species can be an important source of genetic variation because they may arise rapidly, can include multiple mutations on a single haplotype, and have often been pretested by selection in the species of origin. Although introgressed alleles are generally deleterious, several studies have reported introgression as the source of adaptive alleles-including the rodenticide-resistant variant of Vkorc1 that introgressed from Mus spretus into European populations of Mus musculus domesticus. Here, we conducted bidirectional genome scans to characterize introgressed regions into one wild population of M. spretus from Spain and three wild populations of M. m. domesticus from France, Germany, and Iran. Despite the fact that these species show considerable intrinsic postzygotic reproductive isolation, introgression was observed in all individuals, including in the M. musculus reference genome (GRCm38). Mus spretus individuals had a greater proportion of introgression compared with M. m. domesticus, and within M. m. domesticus, the proportion of introgression decreased with geographic distance from the area of sympatry. Introgression was observed on all autosomes for both species, but not on the X-chromosome in M. m. domesticus, consistent with known X-linked hybrid sterility and inviability genes that have been mapped to the M. spretus X-chromosome. Tract lengths were generally short with a few outliers of up to 2.7 Mb. Interestingly, the longest introgressed tracts were in olfactory receptor regions, and introgressed tracts were significantly enriched for olfactory receptor genes in both species, suggesting that introgression may be a source of functional novelty even between species with high barriers to gene flow.
| S-EPMC8784167 | biostudies-literature