Thank you 🙏

And finally:
The effect of SETD2 on transcription is indirect - it likely acts upstream, modulating a plethora of transcription factors. (5/5)

SETD2’s control of readthrough is independent of alternative polyadenylation. It highlights the importance of distinguishing these two processes: 3’ end processing & termination are not the same❗ (4/5)

In cells that don’t have SETD2 or it’s catalytically inactive, readthrough happens because:
1️⃣ TSS initiation is maintained,
2️⃣ 3’ end cleavage is impaired,
3️⃣ cryptic intragenic transcription gets triggered, especially close to the gene ends. (3/5)

We show that SETD2 activity has pleiotropic effects on protein-coding genes:
🟢 promotes proper transcription initiation for most of them (class I),
🛑 stimulates termination in ~20% - prevents transcriptional readthrough (class II). (2/5)

I don't exclude this option :))

Happy to see the first first-author paper from my PhD out! Huge thanks to all co-authors and of course to my brilliant supervisor @stoplab.bsky.social 🙏

Usage of T4ph as a termination marker could benefit more comprehensive genome annotations and help with annotating disease-associated mutations outside of coding regions.

We summarize the findings from literature regarding T4ph and its role in transcription termination. We also provide new analyses that confirm association of T4ph with regions where transcription stops - both at the gene end and prematurely, within the gene body.