heardlab.bsky.social @heardlab.bsky.social · 03/09/20264/ The inactive X can therefore maintain active domains without CTCF/cohesin-dependent loops. Instead, chromatin state itself provides the organizing principle for X-inactivation escape. 000
heardlab.bsky.social @heardlab.bsky.social · 03/09/20263/ So what does hold these domains together? We found that escapee domains are fine-scale chromatin compartments, driven by the spatial clustering of H3K27ac-enriched active chromatin and defined by transitions between opposing chromatin states. 100
heardlab.bsky.social @heardlab.bsky.social · 03/09/20262/ We acutely depleted CTCF and RAD21 in neural progenitor cells with established escape profiles. Despite strongly reducing loop extrusion, escapee gene activity and 3D domain organization remained remarkably stable. No spreading of silencing. No collapse of escape domains. 100
heardlab.bsky.social @heardlab.bsky.social · 03/09/20261/ X-inactivation shuts down most genes on one X chromosome, but some genes escape silencing. These escapees cluster into discrete 3D domains on the inactive X (Xi). So we wondered: are these domains maintained by CTCF and cohesin? 100
heardlab.bsky.social @heardlab.bsky.social · 03/09/2026NEW PREPRINT FROM THE LAB IS OUT — DON’T MISS IT! www.biorxiv.org/content/10.6... We asked whether the 3D architecture of the inactive X - and in particular CTCF and cohesin - is what keeps escapee genes active. Spoiler: it isn’t.biorxiv.orgX-inactivation escapee domains are CTCF-cohesin independent chromatin compartmentsX-chromosome inactivation involves chromosome-wide gene silencing accompanied by extensive chromatin changes, as well the loss of topologically associating domains. Yet discrete regions of the inactiv... 1235
heardlab.bsky.social @heardlab.bsky.social · 03/09/2026A big congratulations to all the authors @agneseloda.bsky.social @antonia-hauth.bsky.social @encent.bsky.social @heard65.bsky.social @mamartirenom.bsky.social 020
heardlab.bsky.social @heardlab.bsky.social · 03/09/2026New preprint from the Heard Lab and the Marti-Renom lab! 🧬 We show that X-inactivation escapee domains form distinct chromatin compartments independently of CTCF and cohesin. www.biorxiv.org/content/10.6...biorxiv.orgX-inactivation escapee domains are CTCF-cohesin independent chromatin compartmentsX-chromosome inactivation involves chromosome-wide gene silencing accompanied by extensive chromatin changes, as well the loss of topologically associating domains. Yet discrete regions of the inactiv... 1285
Reposted by @heardlab.bsky.socialAgnese Loda @agneseloda.bsky.social · 15/12/2025This study was made possible by fantastic collaborations within the @heardlab.bsky.social and beyond. Huge thanks and congratulations to everyone who contributed! 🤩🤩🤩🎉🎉🎉🥳🥳🥳 @odomlab.bsky.social @oliverstegle.bsky.social @howardychang.bsky.social @JudithZaugg 021
Reposted by @heardlab.bsky.socialAgnese Loda @agneseloda.bsky.social · 15/12/2025We propose that natural fluctuations in Xist RNA levels - during development, in adult tissues, or disease - tune escapee gene dosage, laying the groundwork to explore Xist as a molecular signature of X-linked gene mis-regulation in health and disease. 121
Reposted by @heardlab.bsky.socialAgnese Loda @agneseloda.bsky.social · 15/12/2025Xist-mediated repression of escapees is SPEN-dependent and reshapes Xi 3D organization: TAD-like domains over escapee clusters are lost upon silencing and re-emerged when transcription resumes. 101
Reposted by @heardlab.bsky.socialAgnese Loda @agneseloda.bsky.social · 15/12/2025We show that increasing levels of Xist RNA repress escapee genes, well beyond early development, in differentiated, non-dividing cells and in vivo post implantation embryos. 101
heardlab.bsky.social @heardlab.bsky.social · 15/12/2025💡 New paper out in @natcellbio.nature.com 💥💥💥🚀🚀🚀 We uncover an unexpected role for endogenous Xist RNA in regulating X-linked genes that escape X-inactivation well beyond early development, in differentiated, non-dividing cells and in vivo post implantation embryos 👇👇👇👇 1369
