Alan Au

Thanks Max, glad you and your lab enjoyed the paper! Was fortunate to have fantastic colleagues to work with on this project.

Thanks to Inge de Krijger and Michiel Vermeulen for mass spectrometry experiments, Aleksander Szczurek for imaging experiments, and all members of the Klose lab for their support!

Finally, using live-cell transcription imaging (thanks to Aleksander Szczurek), we find that SET1 complexes antagonize the ability of the Restrictor complex to stochastically terminate transcribing polymerases within transcription bursts, thus maintaining burst amplitude.

Using TT-seq, we find that SET1/MLL complex occupancy is required for transcription at over a quarter of all genes, but H3K4me3 is not required. SET1 complexes are the primary effectors of transcription, and do so independently of H3K4me3.

Using degron technology to systematically deplete all SET1/MLL complexes, we find that they synergise to deposit H3K4me3 at gene promoters. Using mass spectrometry (thanks to Inge de Krijger and Michiel Vermeulen), we also identify a novel SET1B isoform that contributes substantially to H3K4me3.

Understanding how H3K4 methylation influences transcription in mammalian cells has been an immense challenge due to the sheer number of H3K4 methyltransferase complexes (6), and also their ability to regulate transcription independently of H3K4 methyltransferase activity.

SET1/MLL complexes control transcription independently of H3K4me3 Histone H3 lysine 4 trimethylation (H3K4me3) at gene promoters is thought to play a central role in gene transcription. H3K4 methylation is deposited by the SET1 (A/B) and MLL (1-4) multi-protein comp...

Excited to share our new preprint from the Klose lab, where we investigate how SET1/MLL complexes shape H3K4me3 and regulate transcription in mouse ES cells. www.biorxiv.org/content/10.6...