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RT @Zhang_Suyang: A transcription balance required for genome stability 🧬⚖️. Our work on RNA Pol II transcription speed control by the DNA….

🛟Wow cyclic peptides are cool! Excited to share a new publication on "Potent Cyclic Peptide Inhibitors Disrupt the FANCM–RMI Interaction". Work led by @yuhenglau to which we contributed structures and ideas. The top hits mimic native MM2. but in reverse!

FANCM is a promising cancer therapeutic target in in ALT-positive or BRCA1, SMARCAL1 & RAD52 negative cancers. Moving toward this goal, our work was an amazing collaboration with industry and academic partners across Australia, China and the UK!.

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 structure, also co-crystallised with splayed DNA shows duplex binding by ERCC4 domain and FAAP24 HhH domains. The two ends of the protein cooperative in recognition of branched DNA substrates at replication forks.

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!

Using our complete biochemical reconstitution system, we show that FANCM stimulates FANCD2/FANCI monoubiquitination by FA core complex in DNA structure-dependent manner. It promotes stable clamp formation even with USP1:UAF1 deubiquitinase present.

🧬New from crystal structures from our lab in EMBO J! We reveal how the FANCM enzyme, an emerging therapeutic target it cancer, has evolved to specifically recognise branched DNA and activate the Fanconi anaemia pathway of DNA repair. 🧵👇.

I'm super excited to announce that registrations are now open for the 19th Australian Cell Cycle, DNA Repair and Telomere Workshop. Awesome international speaker line-up, with plenty of locals being invited! Book now to secure your earlybird rate.

🚀 Scientists, it’s time for a fresh start!🧬.The Twit algorithm is now less on conversation, more on chaos. it’s time to embrace a platform that’s built for connection and collaboration. Join BlueSky and discover a space for real scientific dialogue .#SciTwitter ➡️➡️#BSkySci.

RT @ConstantinouL: We are pleased to inform you that the meeting “From Genome Instability to Cancer: A tribute to Angelos Constantinou” tha….

RT @RichieCDS: I’m thrilled to share this preprint, in which we @BaubecLab engineer DNA damage probes to track DNA damage dynamics by live….

RT @Hedglin_Lab: Check out our latest pre-print, a follow-up to our 2022 NAR study. Now we have characterized encounters of human DNA polym….

RT @aliceyting: In my several decades in science, few moments have been as seismic as when AlphaFold burst onto the scene (seeing the first….

Cool role for replication timing and ATR in aging: "IF aging is due to replication stress induced by cryptic DNA damage, it may explain the conundrum why slowly proliferating tissues, eg liver, age faster than highly proliferating tissues eg intestine."

RT @RogerRogergr: Please us in beautiful Ventura for the 2025 GRC meeting Mammalian DNA Repair: Fundamental Mechanisms to Human Biology ht….