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A cohesin traffic pattern genetically linked to gene regulation [CRISPR screens]

ABSTRACT: Cohesin-mediated loop extrusion is blocked at specific cis-elements, including CTCF sites, producing patterns of loops and domain boundaries along chromosomes. Here, we explore such cis-elements, and their role in gene regulation. We find that transcription termination sites of active genes form cohesin- and RNA polymerase II-dependent domain boundaries that do not accumulate cohesin. At these sites, cohesin is first stalled and then rapidly unloaded. Start sites of transcriptionally active genes form cohesin-bound boundaries, as shown before, but are cohesin-independent. Together with cohesin loading possibly at enhancers, these sites create a pattern of cohesin traffic that guides enhancer-promoter interactions. Disturbing this traffic pattern, by removing CTCF, renders cells sensitive to knock-out of genes involved in transcription initiation, such as the SAGA complexes, and RNA processing such DEAD/H-Box RNA helicases. Without CTCF, these factors are less efficiently recruited to active promoters.

ORGANISM(S): Homo sapiens

PROVIDER: GSE180657 | GEO | 2022/08/15

REPOSITORIES: GEO

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A cohesin traffic pattern genetically linked to gene regulation [Hi-C]

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