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Transcriptional regulation and chromatin architecture maintenance are decoupled functions at the Sox2 locus.

ABSTRACT: Transcriptional regulation and chromatin architecture maintenance are decoupled functions at the Sox2 locus.

PROVIDER: PRJNA802654 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17846300.fastq.gz	Fastqsanger.gz
	SRR17846301.fastq.gz	Fastqsanger.gz
	SRR17846302.fastq.gz	Fastqsanger.gz
	SRR17846303.fastq.gz	Fastqsanger.gz
	SRR17846304.fastq.gz	Fastqsanger.gz

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Transcriptional regulation and chromatin architecture maintenance are decoupled functions at the Sox2 locus.

Project description:How distal regulatory elements regulate gene transcription and chromatin topology is not clearly defined, yet these processes are intimately linked to cell lineage specification during development. Through allele-specific genome editing and chromatin interaction analysis of the Sox2 locus in mouse embryonic stem cells, we found a striking decoupling of transcriptional control and chromatin architecture. We trace nearly all Sox2 transcriptional activation to a small number of key transcription factor binding sites, whose deletion has no effect on promoter-enhancer interaction frequencies or topological domain organization. Local chromatin architecture maintenance, including at the topologically associating domain (TAD) boundary downstream of the Sox2 enhancer, is conversely widely distributed over multiple transcription factor bound regions and maintained in a CTCF independent manner. Furthermore, disruption of promoter-enhancer interactions via induced ectopic chromatin loop formation has no effect on Sox2 expression. These findings indicate many transcription factors are involved in modulating chromatin architecture independently from CTCF.

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Transcriptional regulation and chromatin architecture maintenance are decoupled functions at the <i>Sox2</i> locus.

Project description:How distal regulatory elements control gene transcription and chromatin topology is not clearly defined, yet these processes are closely linked in lineage specification during development. Through allele-specific genome editing and chromatin interaction analyses of the Sox2 locus in mouse embryonic stem cells, we found a striking disconnection between transcriptional control and chromatin architecture. We traced nearly all Sox2 transcriptional activation to a small number of key transcription factor binding sites, whose deletions have no effect on promoter-enhancer interaction frequencies or topological domain organization. Local chromatin architecture maintenance, including at the topologically associating domain (TAD) boundary downstream from the Sox2 enhancer, is widely distributed over multiple transcription factor-bound regions and maintained in a CTCF-independent manner. Furthermore, partial disruption of promoter-enhancer interactions by ectopic chromatin loop formation has no effect on Sox2 transcription. These findings indicate that many transcription factors are involved in modulating chromatin architecture independently of CTCF.

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Project description:The pluripotency transcription factor SOX2 is essential for the maintenance of glioblastoma stem cells (GSC), which drive tumor growth and treatment resistance.To understand how SOX2 is regulated in GSCs, we utilized a proteomic approach and identified the E3 ubiquitin ligase TRIM26 as a direct SOX2-interacting protein. Unexpectedly, we found TRIM26 depletion decreased SOX2 protein levels and increased SOX2 polyubiquitination in patient-derived GSCs, suggesting TRIM26 promotes SOX2 protein stability. Accordingly, TRIM26 knockdown reduced SOX2 transcriptional activity, self-renewal capacity, and in vivo tumorigenicity in multiple GSC lines. Mechanistically, we found TRIM26, via its C-terminal PRYSPRY domain, but independent of its RING domain, stabilizes SOX2 protein by directly inhibiting the interaction of SOX2 with WWP2, which we identify as a bona fide SOX2 E3 ligase in GSCs. Our work identifies E3 ligase competition as a critical mechanism of SOX2 regulation, with functional consequences for GSC identity and maintenance.

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