Chen Davidovich

@davidovichlab.bsky.social

Gene repression, RNA and all chromatin things. @MonashUni, Melbourne, Australia. https://www.davidovich-lab.com/

Preprint alert! 🚨 We are very excited to share our new manuscript on Bohring-Opitz syndrome, a devastating rare monogenic disorder driven by truncating variants in ASXL1. This project was led by PhD student Emma Doyle, one of the OG Conway lab members 💪. 1/6 www.biorxiv.org/content/10.6...

Divergent Pathogenic PR-DUB Complex Variants Converge Functionally Via PRC2 Displacement From Chromatin

The PR-DUB complex is responsible for erasing the repressive histone modification, H2AK119ub1. ASXL1-3 proteins are mutually exclusive catalytic partners of BAP1 in the PR-DUB complex. Somatic heteroz...

biorxiv.org

We’ve recently been awarded a MIRA R35 and an R01 to study non-canonical roles and missense mutations of the Polycomb system in health, cancer, and neurodevelopmental disorders. We are seeking an animal tech with lab manager duties. Please share!

Excited to share our latest work in Molecular Cell: www.cell.com/molecular-ce... We show that PRC1 condensates exclude SWI/SNF from chromatin, revealing a physical mechanism for how opposing regulators compete to control gene expression. Huge thanks to all collaborators and mentors!

Mutual antagonism between PRC1 condensates and SWI/SNF in chromatin regulation

Niekamp et al. show that biomolecular condensates formed by Polycomb repressive complexes can physically restrict access of the activating remodeler SWI/SNF to chromatin. Establishing this barrier dep...

cell.com

☕Neville, Ferguson et al. show that non-canonical Polycomb repressive complex 1.1-mediated gene silencing is antagonized by DOT1L and is required for the therapeutic efficacy of Menin and DOT1L inhibitors in mixed-lineage leukaemia. bit.ly/46MZ3Di

DOT1L provides transcriptional memory through PRC1.1 antagonism - Nature Cell Biology

Neville, Ferguson et al. show that non-canonical Polycomb repressive complex 1.1-mediated gene silencing is antagonized by DOT1L and is required for the therapeutic efficacy of Menin and DOT1L inhibit...

bit.ly

Very excited to share our new Molecular Cell paper on missense mutations in Polycomb genes and how they can disrupt chromatin regulation to drive neurodevelopmental disorders. A huge thank you to everyone involved, and to our amazing collaborators! www.cell.com/molecular-ce...

Unbalanced chromatin binding of Polycomb complexes drives neurodevelopmental disorders

Borges, González-Blanco, Arigela, et al. report new missense mutations in the PRC1 genes RNF2 and RING1 in individuals with neurodevelopmental disorders. Functional dissection of a deleterious variant...

cell.com

www.nature.com/articles/s41... happy i could be a part of this paper from the Gilan lab out now. Along with many other things, it provides strong evidence of chromatin memory for gene activation, and suggests that DOT1L is the missing link balancing the fast and slow arms of the MLL/Polycomb axis

DOT1L provides transcriptional memory through PRC1.1 antagonism - Nature Cell Biology

Neville, Ferguson et al. show that non-canonical Polycomb repressive complex 1.1-mediated gene silencing is antagonized by DOT1L and is required for the therapeutic efficacy of Menin and DOT1L inhibit...

nature.com