Thank you to everyone involved and support from colleagues at @cgen2025.bsky.social and @ucph.bsky.social

Key takeaways:
🔍 Oxidative damage causes an instant shutdown of transcription, but unlike UV, without RNAPII degradation
🔍 Stalled RNAPII resumes transcription from within the gene body
🔍 PARylation controls early elongation restart
🔍 BER and SSBR repair enable RNAPII recovery in the gene body

This beautiful work, led by Quentin Thomas, revealed a surprising spatial organization of the transcriptional response:

🔬 Promoter regions: PARylation governs early RNAPII release
🔬 Gene body: DNA damage and repair drive RNAPII stalling

Huge thanks to our amazing team and members within @cgen2025.bsky.social for fruitful discussions 🙌

What did we find? ✅ Elongation rates vary between genes ✅ …and within genes ✅ Histone marks & elongation factors correlate with rate subclasses

Existing methods either rely on indirect estimates or are limited to a handful of long genes. So we built DRB/TTchem-seq2: Short timepoint sampling, new computational framework 📈 leading to a ~7 fold increased individual gene elongation rates measurements!