Andrew Deans

ATP-dependent remodeling of chromatin condensates reveals distinct mesoscale outcomes Adenosine triphosphate (ATP)–dependent chromatin remodeling enzymes mobilize nucleosomes, but how such mobilization affects chromatin condensation is unclear. We investigate effects of two major remod...

Today I am so pleased to present our work on how chromatin remodelers affect mesoscale chromatin organization.
www.science.org/doi/10.1126/...

Australian Cell Cycle, DNA repair and Telomere meeting draft schedule is now online!
Join us with 5 plenary speakers, 16 invited national speakers, 22 selected speakers, 61 poster presenters and lots and lots of fun science. Less than one month to go.
australiancellcycle.org/draft-schedu...

Differential PARP inhibitor responses in BRCA1-deficient and resistant cells in competitive co-culture Synthetic lethality describes a genetic relationship where the loss of two genes results in cell death, but the loss of one of those genes does not. Drugs used for precision oncology can exploit synth...

Happy to share the latest paper from the lab looking at PARP inhibitor responses in isogenic BRCA1 cell line pairs, from the Master work of Shiella Amelia Soetomo and Michael Sharp: dx.plos.org/10.1371/jour...

The Eukaryotic homology search complex distorts donor DNA structure to probe for homology Homologous recombination (HR) is a DNA double-strand break repair pathway that facilitates genetic exchange and protects damaged replication forks during DNA synthesis. As a template-based repair proc...

Just throwing this out there as a significant conceptual advance in the field

www.biorxiv.org/content/10.1...

A high-resolution, nanopore-based artificial intelligence assay for DNA replication stress in human cancer cells Nature Communications - Determining how replication forks move across the human genome is critical for the effective use of agents that target replication stress. Here, the authors present...

Checkout our latest research in @natcomms.nature.com
rdcu.be/eBqBI A high-resolution, nanopore-based artificial intelligence assay for DNA replication stress in human cancer cells. A collaboration with Mike Boemo’s team

Australian Invited Speakers 2025 We are in the process of inviting a number of outstanding Australian leaders in the fields of DNA repair, Cell Cycle and Telomere biology. Current invited speakers include: Lisa Alcock, Curtain Uni…

🦘🧬Australian invited speaker list finalised for the
2025 Cell Cycle, DNA repair and Telomere Meeting!
Friday 5 Sep is your last chance to register at the EARLY BIRD rate & submit an abstract 🤩
australiancellcycle.org/australian-i...

🚨 Last chance! Register NOW for the Australian Cell Cycle, DNA Repair & Telomere Meeting 🧬
📍 Melbourne Museum | Oct 19–22
Submit your abstract + lock in the reduced rate this week
👉 australiancellcycle.org

Registering some members of my team for the 19th Australian Cell Cycle, DNA Repair and Telomere Workshop in Melbourne in October. Early-bird registrations by August 31. 🧪

High-throughput investigation of cyclin docking interactions reveals the complexity of motif binding determinants - Nature Communications Many protein–protein interactions depend on Short Linear Motifs (SLiMs). In this study, the authors use large-scale binding assays, deep mutational scanning, and structural analysis to map SLiMs recog...

Just published: Our paper on high-throughput analysis of cyclin docking interactions, led by the group of Norman Davey @icr.ac.uk and with some small-complex-plus-peptide #cryoEM by @natalia-mg.bsky.social from my lab. Congratulations, everyone!
www.nature.com/articles/s41...

Heads up for those working in ubiquitin biology and targeted protein degradation—Lorne Ubiquitin 2025 is happening 20–23 November in Lorne, Victoria, Australia.

Late abstracts are still being accepted—worth checking out if you’re looking to share your work in a focused, international setting. 🦘🦘🦘

New from us in @natrevmcb.nature.com -- @szmyd-radoslaw.bsky.social & @radoncdocgee.bsky.social explore how DNA repair actively shapes cancer cell fate following DNA damage, reframing repair as both a protective process & a driver of treatment response and cell death. www.nature.com/articles/s41...

In case you missed the online advance version, we are now in the latest print issue of EMBO J! www.embopress.org/doi/full/10.... Structural and biochemical investigation of the key activation step in the Fanconi anaemia DNA repair pathway, recognition of branched DNA by FANCM

Image credit: @gloglita.bsky.social‬ @lifescienceeditors.bsky.social‬ captured DynaTag in action: a pA-Tn5 probe (multicoloured) binds an antibody (white), which binds p53 DNA-binding domain (green) on DNA (blue) within 2 nucleosomes

🧪Move over CUT&Tag, there’s a new #TranscriptionFactor mapping method in town.
Our newly developed DynaTag is faster, cleaner, more sensitive than #ChIPseq, #CUT&RUN and #CUT&Tag.
🔗 Our @natcomms.nature.com paper: www.nature.com/articles/s41...
🧵Let’s break down what makes DynaTag so powerful (1/7)

This was my all time favourite conference to attend anywhere in the world. Almost makes me wanna get back into research just so I can attend.

Australian Cell Cycle, DNA repair and Telomere Meeting October 20-22, 2025

Register for the Australian Cell Cycle, DNA Repair & Telomere Meeting in beautiful Melbourne October 19-22, 2025. Plenty of slots for selected abstracts and posters. High praise last time from Piotr Sicinski: "en par with a Gordon conference for science and interaction"
www.australiancellcycle.org

Waiting for reviews: 'This is taking forever!' 😤
Doing reviews: 'Extension please?' 🙃

Identification of RNF114 as ADPr-Ub reader through non-hydrolysable ubiquitinated ADP-ribose - Nature Communications Deltex E3s modify ADP-ribosylated targets with ubiquitin, creating a hybrid modification whose readers remains unknown. Here, the authors synthesise a non-hydrolysable probe that mimics the modificati...

A few years back we discovered a dual hybrid protein modification composed of ADP-ribose dinucleotide and ubiquitin (ADPr-Ub). Now we reveal that ADPr-Ub can be further ubiquitinated by the E3 ubiquitin ligase RNF114!
www.nature.com/articles/s41...

www.science.org/doi/10.1126/...

Symington lab Preprint: Evidence for asymmetrical resection at replication-associated DSBs:
www.biorxiv.org/content/10.1...

Check out this new review (with animations, natch) of mechanisms of licensing origins of DNA replication - a wonderful (and continuing!) collaboration with Bruce Stillman @cshlnews.bsky.social and John Diffley @crick.ac.uk! www.nature.com/articles/s41...

Really cool new cryoEM structure of RAD51 caught in the act of recombination initiation at a D-loop. elifesciences.org/reviewed-pre...

Potent Cyclic Peptide Inhibitors Disrupt the FANCM–RMI Interaction FANCM–RMI is a protein–protein interaction that maintains genome stability during DNA repair events in cancers that rely on the Alternative Lengthening of Telomeres (ALT) pathway for survival. We repo...

💥🛟Wow cyclic peptides are cool! So excited to share a new publication on "Potent Cyclic Peptide Inhibitors Disrupt the FANCM–RMI Interaction". Work led by @yuhenglau.bsky.social to which we contributed structures and ideas. The top hits mimic native MM2...but in reverse! pubs.acs.org/doi/10.1021/...

BRCA2 C-terminal clamp restructures RAD51 dimers to bind B-DNA for replication fork stability With detailed structural and molecular analyses, Longo et al. find that the BRCA2 C-terminal TR2, which is a critical cancer therapy resistance factor, reshapes the RAD51 dimer for B-DNA binding that ...

BRCA2 C-terminal clamp restructures RAD51 dimers to bind B-DNA for replication fork stability: Molecular Cell www.cell.com/molecular-ce...

Andrew Deans @genomestability.bsky.social and collaborators show that #FANCM helicase has evolved from an ancient repair motor into a specialized sensor coupling DNA-damage recognition to Fanconi Anemia pathway activation
www.embopress.org/doi/full/10....

Structural basis of Fanconi anemia pathway activation by FANCM | The EMBO Journal imageimageFANCM employs a sophisticated dual recognition mechanism in genome maintenance, using distinct DNA-binding domains to identify and move around on branched DNA structures. This study reveals how FANCM evolved from an ancient repair motor ...

FANCM is a promising cancer therapeutic target due to genetic interactions with BRCA1, SMARCAL1 & RAD52 & in ALT-positive cancers. Moving toward this goal, our work was an amazing collaboration with industry and academic partners across Australia, China and the UK!
www.embopress.org/doi/full/10....

Instead, a different part of FANCM is required, the MM1 domain. We used AlphaFold modelling to show that the MM1 domain grabs onto the FA core complex binding and mutants in this domain also fail to repair DNA damage properly.

Structure-specific DNA binding, not ATP hydrolysis, is required for FANCD2:FANCI monoubiquitination.

🧩 We also have a new structure of FANCM-CTD:FAAP24, also co-crystallised with splayed DNA. The two ends of the protein cooperative in recognition of branched DNA substrates at replication forks and other DNA junctions.

But FANCM arranges itself on DNA very differently. Using a brand new DNA migration assay we show that several key DNA-binding residues contact the DNA junction (green), while others (yellow) grab onto the splayed DNA so that ATP hydrolysis is converted to forward momentum.

Actually, the protein has evolved from the same ancestor as the dsRNA immune receptor proteins RIG-I and MDA-5, and the siRNA processing enzyme Dicer, and the DNA repair protein XPF.

And here is what FANCM translocase domain bound to 3'flap hairpin DNA looks like!