𝗖𝗮𝗻 𝗰𝗲𝗹𝗹𝘀 𝗲𝘃𝗲𝗿 𝘁𝗿𝘂𝗹𝘆 𝗿𝗲𝗰𝗼𝘃𝗲𝗿 𝗳𝗿𝗼𝗺 𝗗𝗡𝗔 𝗱𝗮𝗺𝗮𝗴𝗲?Excited to share our new study “Repair of DNA double-strand breaks leaves heritable impairment to genome function”, revealing DNA repair’s hidden cost, out now @science.org tinyurl.com/5n6zw3ye. Led by @sbantele.bsky.social and Jiri Lukas.🧵👇1/n

Repair of DNA double-strand breaks leaves heritable impairment to genome function

Upon DNA breakage, a genomic locus undergoes alterations in three-dimensional chromatin architecture to facilitate signaling and repair. Although cells possess mechanisms to repair damaged DNA, it is ...

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𝐍𝐞𝐰 𝐦𝐞𝐜𝐡𝐚𝐧𝐢𝐬𝐭𝐢𝐜 𝐢𝐧𝐬𝐢𝐠𝐡𝐭𝐬 𝐢𝐧𝐭𝐨 𝐭𝐡𝐞 𝐫𝐞𝐠𝐮𝐥𝐚𝐭𝐢𝐨𝐧 𝐨𝐟 𝐡𝐢𝐬𝐭𝐨𝐧𝐞 𝐬𝐮𝐩𝐩𝐥𝐲! Excited to share our latest collaboration led by tkjeong.bsky.social and ciaranfrater.bsky.social! Structural determination of the histone chaperone ASF1 and its regulator CODANIN-1 uncovers how CODANIN-1 counters ASF1 activity. 🧵👇

CODANIN-1 sequesters ASF1 by using a histone H3 mimic helix to regulate the histone supply

Nature Communications - CODANIN-1 negatively regulates the function of ASF1, the key chaperone for histone H3-H4 supply. Here the authors present the cryo-EM structure of the CODANIN-1_ASF1A...

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SAVE THE DATE! The next EMBO | EMBL Symposium on 'DNA replication and genome maintenance: from basic biology to disease' will be held October 20-23, 2026.   Organized by Helle Ulrich (IMB), Johannes Walter (Harvard) and Anja Groth (Danish Cancer Institute). www.embl.org/about/info/c...

𝐇𝐨𝐰 𝐝𝐨 𝐜𝐞𝐥𝐥𝐬 𝐫𝐞𝐦𝐞𝐦𝐛𝐞𝐫 𝐰𝐡𝐨 𝐭𝐡𝐞𝐲 𝐚𝐫𝐞 𝐚𝐟𝐭𝐞𝐫 𝐃𝐍𝐀 𝐫𝐞𝐩𝐥𝐢𝐜𝐚𝐭𝐢𝐨𝐧? Our new study “Disabling leading and lagging strand histone transmission results in parental histones loss and reduced cell plasticity and viability” is out in 𝘚𝘤𝘪𝘦𝘯𝘤𝘦 𝘈𝘥𝘷𝘢𝘯𝘤𝘦𝘴. Led by @lleonie.bsky.social @biranalva.bsky.social 🧵 More below👇

Disabling leading and lagging strand histone transmission results in parental histones loss and reduced cell plasticity and viability

Losing parental histones during DNA replication fork passage challenges differentiation competence and cell viability.

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Excited to share the first of 2 new papers diving into functions of UHRF1 ubiquitin ligase activity. Here, a connection to the support of 5mC maintenance in regions of low CpG density. These same regions are prone to 5mC loss in cancer. A potential mechanistic link to PMD formation. #epigenetics

UHRF1 ubiquitin ligase activity supports the maintenance of low-density CpG methylation

Abstract. The RING E3 ubiquitin ligase UHRF1 is an established cofactor for DNA methylation inheritance. The model posits that nucleosomal engagement throu

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Single cell genomics was a breakthrough in understanding cancer heterogeneity. Incredible work by Lucas et al. in breaking the next barrier, cancer proliferation heterogeneity tinyurl.com/mjuuk7kt Honoured I was invited to write the News&Views. tinyurl.com/yc27a4ac Both out now in Nature Genetics!

Characterizing the evolutionary dynamics of cancer proliferation in single-cell clones with SPRINTER - Nature Genetics

Single-cell Proliferation Rate Inference in Non-homogeneous Tumors through Evolutionary Routes (SPRINTER) allows users to infer proliferation rates of individual clones within a tumor from single-cell...

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