🧬 This work was a team effort from the Stewart-Morgan, Brickman & Groth labs👩‍🔬👨‍🔬🧑‍🔬 - great to see it now published! 📝 🥳

Post-replicative chromatin accessibility predicts cell fate change Knudsen and colleagues use repli-ATAC-seq to compare replicated and unreplicated chromatin in two models of cell identity change. They find that lineage-specific elements are accessible earlier in rep...

DNA replication globally disrupts the epigenome. But does this create a chromatin-access opportunity for TF binding to facilitate cell identity change? Now 𝐫𝐞𝐩𝐥𝐢-𝐀𝐓𝐀𝐂-𝐬𝐞𝐪 shows 𝘥𝘦 𝘯𝘰𝘷𝘰 chromatin opening & TF binding occurs specifically post-replication, in cellular differentiation & reprogramming!

Biomedicine prize awarded to Professor Anja Groth for groundbreaking discoveries in epigenetic cell memory - Novo Nordisk Fonden

You can read more about Anja's award here: novonordiskfonden.dk/en/news/biom...

A picture of current members of the Groth lab

Congratulations to @groth-anja.bsky.social on receiving the Novo Nordisk Foundation Jacobæus Prize 🏆 we’re proud to see Anja's mentorship, leadership, & pioneering work in epigenetic cell memory getting top recognition 👏 celebrating the contributions of past & present lab members to this work too 🥳

Our latest collaboration with the talented Susi @sbantele.bsky.social and Jiri Lukas is out now @science.org 🤩. We reveal the hidden price for DNA repair, with potential implications for genome function, gene therapy and ageing👇

It was wonderful to hear talks from EpiC members @grothlab.bsky.social @nilskrietenstein.bsky.social @nilssonlab.bsky.social & Niels Mailand, now we are settled in our new home @cancer.dk. We are grateful for @dg.dk for this exciting opportunity. Onwards and upwards with EpiC science! 🧬 #CPRLegacy

Image of Niels Mejlgaar (CEO of DNRF), Anja Groth (EpiC director) & Jesper Fisker (CEO of DCS).

We have lift off!! 🚀 Yesterday was the official opening of EpiC! The DNRF Center for Epigenetic Cell Memory at the Danish Cancer Institute!
Our EpiC team with director Anja Groth @groth-anja.bsky.social, were joined by Jesper Fisker, CEO @cancer.dk & Niels Mejlgaar, CEO @dg.dk to celebrate 🎉

Postdoctoral Fellow - Costa Lab Salary for this Role: From £45,500 with benefits, subject to skills and experience. Job Title: Postdoctoral Fellow - Costa Lab Reports to: Alessandro Costa Closing Date: 03/Aug/2025 23.59 GMT Job Desc...

Less than two weeks left to apply!

Postdoc positions in my lab to study

1. initiation of DNA replication.

2. chromatin replication/epigenetic inheritance.

Great for biochemists, biophysicists & structural biologists.

Deadline 3 August 2025.

crick.wd3.myworkdayjobs.com/External/job...

Congratulations to Ada 🥳🍾, who very successfully defended her master's thesis today! You were an excellent student and we were super happy to have you in the lab! Wishing you all the best for the future and enjoy your well-deserved break!

Postdoc positions open in my lab (Francis Crick Institute) to study

1. initiation of DNA replication.

2. chromatin replication/epigenetic inheritance.

Great for biochemists, biophysicists and cryo-EM/cryo-tomography scientists.

Deadline 3 August 2025.

crick.wd3.myworkdayjobs.com/External/job...

🚨 Postdoc wanted (🇳🇱NL based) for our exciting collaboration with the lab of Alexander van Oudenaarden @hubrechtinstitute.bsky.social in Utrecht, with collaborative visits to our lab Copenhagen 🇩🇰. We seek a computational scientist to model epigenetic inheritance, see more below 👇!

Welcome Marcel!!

Thank you, Tae-Kyeong!

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...

Together our work gives a molecular basis for histone supply regulation by CODANIN-1, read the full paper here: rdcu.be/ecbHq . Thanks to the Song lab at KAIST jijoonsong.bsky.social for taking us onboard as collaborators for this exciting new structure-function adventure!

How important is CODANIN/ASF1A complex formation? Inhibiting dimerization in cells or introducing a pathogenic CDA-I mutation in the dimerization interface reduced ASF1A cytoplasmic sequestration. This shows the significance of CODANIN/ASF1A complex formation and possible disease relevance

Which CODANIN binding sites are required for ASF1 regulation? Using inducible complementation of CODANIN-1 in cells, we found that mutation of both BD-N and HMH-C is needed to prevent cytoplasmic sequestration of ASF1A. Thus, CODANIN-1 regulates ASF1A nuclear import by this dual-binding mechanism.

By binding in this way, CODANIN-1 occludes the two major histone-binding surfaces of ASF1A, preventing its chaperone activity. Interestingly, CODANIN-1 could also bind preformed ASF1A/H3-H4 using its B domains, suggesting that it may regulate ASF1 at multiple points in the histone supply chain.

So, how does CODANIN-1 bind ASF1? Our cryo-EM structure reveals that CODANIN-1 forms a dimer, with each monomer binding two ASF1A molecules. These two ASF1As are held in proximal and distal positions by CODANIN’s N-terminal B domain (BD-N) and C-terminal histone H3 mimic helix (HMH-C), respectively.

A bit of background: ASF1 plays a central role in histone nuclear import and supply for replication & transcription. CODANIN-1 is commonly mutated in a rare form of heritable anaemia (CDA-I) and inhibits histone supply by ASF1. But we don’t currently understand these roles on the molecular level.

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...

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. 🧵👇

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...

Epigenetics Gordon Research Conference. Consider joining us for what will be an excellent, exciting meeting and will be held in Europe for the first time: 10-15 Aug25 Barcelona, Spain. Please repost and apply early - this meeting is popular! www.grc.org/epigenetics-...

Transcription-replication conflicts drive R-loop-dependent nucleosome eviction and require DOT1L activity for transcription recovery Abstract. Progressing transcription and replication machineries profoundly impact their underlying chromatin template. Consequently, transcription-replicat

I am delighted to share the main work of my PhD project in the @hamperllab.bsky.social now out in @narjournal.bsky.social. TRCs drive R-loop-dependent nucleosome eviction and require DOT1L activity for transcription recovery.
academic.oup.com/nar/article/...

#TRC #r-loop #chromatin

More below 👇

Thank you, Jeroen!

6 Postdoctoral and PhD positions in Center for Epigenetic Cell Memory (EpiC) The Center for Epigenetic Cell Memory (EpiC) is a new Center of Excellence that will be established based on funding by the Danish National Research Foundation.

If you’re interested in epigenetic inheritance and cell division, check out the vacancies for 6 PhDs and Postdocs positions in our new Center for Epigenetic Cell Memory (EpiC): tinyurl.com/yvd93na2 6/n

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.

Want to dive deeper? 🧐 Read the full paper here: tinyurl.com/233y89d2 🔗📖. Last, a big thank you to all our collaborators and colleagues at #NNF-CPR 🙏. #HistoneRecycling #Epigenetics #Chromatin #ScienceAdvances 5/n

Our work highlights 𝐩𝐚𝐫𝐞𝐧𝐭𝐚𝐥 𝐡𝐢𝐬𝐭𝐨𝐧𝐞 𝐫𝐞𝐜𝐲𝐜𝐥𝐢𝐧𝐠 𝐚𝐬 𝐚 𝐤𝐞𝐲 𝐞𝐩𝐢𝐠𝐞𝐧𝐞𝐭𝐢𝐜 𝐬𝐚𝐟𝐞𝐠𝐮𝐚𝐫𝐝 – histone modifications must be 𝐞𝐟𝐟𝐢𝐜𝐢𝐞𝐧𝐭𝐥𝐲 transmitted to 𝐛𝐨𝐭𝐡 daughter strands for this to work! Could failures in this process contribute to developmental disorders, cancer, or aging? More to explore! 4/n

What happens next? Gene misregulation & differentiation defects start to emerge. But when 𝐛𝐨𝐭𝐡 leading & lagging strand recycling are disrupted (POLE4 & MCM2-2A), 𝐬𝐨𝐦𝐞 𝐩𝐚𝐫𝐞𝐧𝐭𝐚𝐥 𝐡𝐢𝐬𝐭𝐨𝐧𝐞𝐬 𝐚𝐫𝐞 𝐥𝐨𝐬𝐭 𝐢𝐧 𝐭𝐫𝐚𝐧𝐬𝐦𝐢𝐬𝐬𝐢𝐨𝐧 —worsening the defects. Unlike single mutants, cells now start to die! 3/n

We use a degron to deplete POLE4, a leading strand recycler, in WT or a background defective in lagging strand recycling (MCM2-2A). The first epigenome alteration upon acute loss of leading strand recycling is 𝐚𝐜𝐜𝐮𝐦𝐮𝐥𝐚𝐭𝐢𝐨𝐧 𝐨𝐟 𝐇𝟑𝐊𝟐𝟕𝐦𝐞𝟑 - 𝐰𝐢𝐭𝐡𝐢𝐧 𝟏-𝟐 𝐜𝐞𝐥𝐥 𝐜𝐲𝐜𝐥𝐞𝐬 - 𝐛𝐞𝐟𝐨𝐫𝐞 𝐭𝐫𝐚𝐧𝐬𝐜𝐫𝐢𝐩𝐭𝐢𝐨𝐧𝐚𝐥 𝐜𝐡𝐚𝐧𝐠𝐞𝐬! 2/n

During replication, modified parental histones are transmitted to the daughter DNA strands - they are recycled. Recycled histones serve as agents of memory to maintain the epigenome in daughter cells! What happens when recycling is acutely disrupted? 1/n