Oh! Would have been great to see you (I live in Wollongong now). But I am off to Korea tomorrow! Enjoy the gong. Hope the weather improves. 🤞

Great list! Can I be added too please?

Also take a look at complementary work from Jesper Svejstrup's lab:
sciencedirect.com/science/arti...

Thanks to support from @singmolsci.bsky.social @unswrna.bsky.social

When both ARMC5 and INTS8 are depleted, excess Pol II is released into genes but often fails to transcribe the full transcription unit, resulting in major gene expression changes. There is lots more in the paper, of course!

This finding pushed us to try to understand what stops Pol II from entering the elongation phase and actually making more RNA. We found that ARMC5 and Integrator phosphatase play complementary roles in this process.

ARMC5 also regulates Pol II levels during normal cell growth - seemingly responsible for around half the cell’s Pol II turnover. But the extra Pol II that accumulates in cells upon ARMC5 loss doesn’t lead to more Pol II in gene bodies: it is mostly in the free pool or in the proximal promoter.

However, using live-cell imaging and cellular fractionation, we found that this excess Pol II mostly accumulates off-chromatin.

It has long been known that Pol II is degraded when transcription is inhibited - either with small molecules or if specific cofactors are depleted. We now know the ubiquitin ligase responsible is CUL3-ARMC5. When we remove ARMC5, Pol II is no longer lost upon inhibition.

Building on our previous work on RNA concentration homeostasis doi.org/10.1016/j.ce..., we were interested to understand how global levels of Pol II are controlled. We teamed up with @anatv.bsky.social's lab who delve deep into mechanisms of ubiquitin-mediated regulation of the transcription cycle.