Inlay

Post doc at @FMIscience in the Chao lab | formerly @PeterMacCC | Views are my own

Proud to share our paper on the impact of transcription inhibition on mRNA export in cancer. A big thanks to collaborators, especially to Ewa Michalak, Vi Wickramasinghe, Jeff Chao and Mark Dawson @mafdawson.bsky.social. @fmiscience.bsky.social

I am very excited to share our most recent work on how ‘Cell heterogeneity and fate bistability drive tissue patterning during intestinal regeneration’ ☺️ Thanks a lot to @silviabarbiero.bsky.social @davidbrueckner.bsky.social @priscaliberali.bsky.social @ehannezo.bsky.social and all the co-authors!

Are you a bioinformatician looking for an exciting opportunity in Melbourne? Is cancer genomics your passion? Apply now! www.nature.com/naturecareer...

One week left to send your application for the image analyst position. If you are interested, apply!

📖 Happy to share our recent preprint! www.biorxiv.org/content/10.1... We discovered how SINEs are kept silent: the ChAHP protein complex acts as a molecular brake on POL III transcription retrotransposons. A 🧵:

🧵 New preprint! How does a chromatin remodeler know where to act? In our latest study, we show how the transcription factor ADNP targets CHD4 remodeling activity to silence transposons and block CTCF. 👇 A thread on the ChAHP complex and how it weaves chromatin 🧬🔬🧵 www.biorxiv.org/content/10.1...

Jakob Schnabl-Baumgartner

Why can a human tolerate a drug that globally inhibits transcription? Why do transcription inhibitors not cure cancer? Our first paper of 2025 may help explain (some) of this! So incredibly proud of @tobiaswilliams.bsky.social & Ewa Michalak who led the work! www.cell.com/molecular-ce...

Exciting opportunity to join a research program led by Sarah-Jane Dawson at the Peter MacCallum Cancer Centre (www.thedawsonlab.com).

A perfect start in the new year! 🌱 Regenerating tissues are just an amazing spatio temporal controlled process! Our new manuscript explores how cell heterogeneity and bistability orchestrate intestinal regeneration. 🧵 biorxiv.org/cgi/content/...

Short interspersed nuclear elements (SINEs) are abundant non-autonomous transposable elements derived from RNA polymerase III (POL III)-transcribed short non-coding RNAs. SINEs retain sequence feature...

Transcription inhibitors also disrupt nuclear export. Here, Williams et al. reveal that mRNA export factors sense transcription inhibition and adapt by storing mature export-competent mRNA in nuclear speckles. This enables rapid release when transcription resumes and ensures retention of cellular identity and viability during a transient global transcription insult.

🚨Job alert: We're hiring a Data Scientist (Image Analysis) to join our Facility for Advanced Imaging & Microscopy. The facility provides cutting-edge light and electron microscopy, high-content screening, image analysis and spatial-transcriptomics services. Apply at: www.fmi.ch/education-ca...

Tissue regeneration relies on the ability of cells to undergo de novo patterning. While tissue patterning has been viewed as the transition from initially identical un-patterned cells to an arrangemen...

Transcription in eukaryotes is regulated by chromatin-based mechanisms that control nucleosome occupancy, chromatin modifications, and transcription factor binding. We have previously shown that the transcription factor ADNP forms the ChAHP complex with the chromatin remodeler CHD4 and HP1 proteins, acting as a site-specific regulator of transcription and antagonist of CTCF binding. However, the molecular basis of these functions remained unclear. Here, we demonstrate that the CHD4 subunit is essential to antagonize CTCF and silence transcription of transposons, while HP1 proteins are dispensable. Although the remodeling activity of CHD4 is not required for ChAHP chromatin association, it is critical for both transposon repression and CTCF antagonism. Our findings support a model wherein ADNP recruits chromatin remodeling activity in a sequence-specific manner, enabling transcriptional control and local modulation of chromatin architecture. ### Competing Interest Statement The Friedrich Miescher Institute for Biomedical Research (FMI) receives significant financial contributions from the Novartis Research Foundation. Published research reagents from the FMI are shared with the academic community under a Material Transfer Agreement (MTA) having terms and conditions corresponding to those of the UBMTA (Uniform Biological Material Transfer Agreement). Novartis Research Foundation, n.a. Swiss National Science Foundation, grant 310030_188835