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Biology subjects

Carel, I.

Publications and source records attributed to Carel, I..

2 recordsLinked to original sources

Cohesin bridging as a physical principle of enhancer-promoter communication

Central to genome function, enhancers are non-coding sequences that can control transcription from promoters hundreds of kilobases away. Yet the physical basis of this long-range communication remains unclear. A prevalent view is that enhancers activate promoters when the two elements come into spatial proximity through the 3D folding of chromatin. However, activation by spatial proximity alone has struggled to explain several core features of enhancer function. Here, we propose that the molecular motor cohesin transmits long-range enhancer action by forming bridges between enhancers and promoters during loop extrusion. In this view, rare and transient bridges carry regulatory communication, rather than mere spatial proximity. We develop a quantitative model that predicts transcriptional output from cohesin-bridging dynamics and validate it by engineering cells in which strategically positioned CTCF sites rewire loop extrusion trajectories. The model explains how enhancer action scales with genomic distance, and how it can be either facilitated or insulated by CTCF sites across two orders of magnitude-behaviors incompatible with proximity-based models. Finally, our framework reveals that CTCF sites can block enhancers bidirectionally, by either blocking or releasing cohesin loops, resolving longstanding paradoxes between their effects on transcriptional regulation and genome folding. Together, our results establish cohesin bridging as a mode of enhancer-promoter communication that can be modulated by genomic context to achieve selective and tunable transcriptional control over long genomic distances.

molecular biology↗

Synergy between cis-regulatory elements can render cohesin dispensable for distal enhancer function

Enhancers are critical genetic elements controlling transcription from promoters, but the mechanisms by which they convey regulatory information across large genomic distances remain elusive. Here, we engineered pluripotent stem cells in which cohesin loop extrusion can be inducibly disrupted without causing confounding cell cycle defects. While evident, transcriptional dysregulation was cell-type specific, and not all loci with distal enhancers depend equally on cohesin extrusion. Using comparative genome editing, we demonstrate that enhancer-promoter communication across as little as 20 kilobases can rely on cohesin. However, promoter-proximal regulatory elements can support long-range, cohesin-independent enhancer action - either upon disabling extrusion or across strong CTCF insulators. Finally, transcriptional dynamics and the emergence of new embryonic cell types in response to differentiation cues remained largely robust to disrupting cohesin extrusion. Beyond establishing novel experimental strategies to study cohesin functions in enhancer biology, our work provides mechanistic insight accounting for both cell type- and genomic context-specificity.

molecular biology↗