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Interplay of EGFR signaling and ARID1A in regulating transcriptome of celllular-plasticity genes

ABSTRACT: Interplay of EGFR signaling and ARID1A in regulating transcriptome of celllular-plasticity genes

PROVIDER: PRJNA700521 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13649685.fastq.gz	Fastqsanger.gz
	SRR13649686.fastq.gz	Fastqsanger.gz
	SRR13649687.fastq.gz	Fastqsanger.gz
	SRR13649688.fastq.gz	Fastqsanger.gz
	SRR13649689.fastq.gz	Fastqsanger.gz

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Interplay of EGFR signaling and ARID1A in regulating transcriptome of celllular-plasticity genes

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Protein proximity analysis unravels a complex interplay between lymphoid transcription factors and ARID1a in T-cell development.

Project description:Maturation of lymphoid cells is controlled by the action of stage and lineage restricted transcription factors, which work with the general transcription and chromatin remodelling machinery to regulate gene expression. To better understand this functional interplay we used BioID to identify proximity interaction partners for GATA3, TCF7, SPI1, HLF, IKZF1, PAX5, ID1 and ID2. We found that ARID1a, a BAF complex component, interacts with a number of these transcription factors. Consistent with this observation, deletion of Arid1a in early lymphoid progenitors resulted in reduced production of IgM+ immature B-cells, a pronounced block in early T-cell development, a 10-fold reduction in thymic cellularity, a reduction in CD4+CD8+ cells, and a developmental arrest in the DN3 to DN4 transition. Our work highlights the critical importance of functional interactions between stage and lineage restricted factors and the basic transcription machinery during lymphocyte differentiation.

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ChIP-seq analysis of Arid1a and C/ebpÎ± in the mouse livers

Project description:Arid1a is the subunit of SWI/SNF complex, which was reported to guide SWI/SNF to DNA. Here, we found that loss of Arid1a in the liver and other adult tissues results in improved organ regeneration. Within SWI/SNF complexes, Arid1a physically interacts with C/ebpÎ±, a hepatocyte transcription factor that drives maturation and limits proliferation. Genome-wide analysis showed that loss of Arid1a reduces the recruitment and activity of C/ebpÎ± on target promoters, resulting in expression programs that favor regeneration and cellular fitness during injury. Arid1a binding is enriched in promoters near transcriptional start sites (TSSs), and C/ebpÎ± binds at precisely the same positions, indicating that Arid1a facilitates C/ebpÎ± binding across the genome. Perfuse and isolate primary hepatocytes from mice livers, analysis of genomic occupancy of C/ebpÎ± and H3K4me2 in hepatocytes from Arid1a WT and Arid1a liver specific KO mice by ChIP-seq. Analysis of genomic occupancy of Arid1a in the hepatocytes from V5-Arid1a transgenic mouse by ChIP-seq.

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