Konrad Chudzik

The cover of Nature Genetics July 2025 issue. Digital art of a mouse paw skeletal prep on dark background, digits I to IV disintegrating into viral particles. A caption says “An endogenous retrovirus causes limb malformation”.

Pretty surreal to see my artwork on the cover of Nature Genetics! Big congrats to @julianeg.bsky.social, @stemundi.bsky.social and the others, and thank you Juliane for letting me help bring your research to life visually.

www.nature.com/ng/volumes/5...

The nuclear periphery confers repression on H3K9me2-marked genes and transposons to shape cell fate - Nature Cell Biology Marin et al. report the role of lamin proteins and the lamin B receptor (LBR) in chromatin positioning at the nuclear periphery. Knockout of all lamins and LBR in mouse embryonic stem cells leads to h...

Another paper bluetorial! Today: how does the spatial location of genes influence their function? (1/n) www.nature.com/articles/s41...

Retrospective and multifactorial single-cell profiling reveals sequential chromatin reorganization during X inactivation - Nature Cell Biology Kefalopoulou, Rullens et al. develop Dam&ChIC to assay chromatin state at two different time points in the same cell. The method was used to study the reorganization of LADs during cell division a...

I am very excited to share our latest work where we describe a new method to profile genome-wide chromatin transitions over time in single cells. Great collaborative effort with the van Oudenaarden group @hubrechtinstitute.bsky.social @oncodeinstitute.bsky.social www.nature.com/articles/s41....

Enhancer adoption by an LTR retrotransposon generates viral-like particles, causing developmental limb phenotypes - Nature Genetics Activation of an LTR retrotransposon inserted upstream of the Fgf8 gene produces viral-like particles in the mouse developing limb, triggering apoptosis and causing limb malformation. This phenotype c...

Finally out! 🥳 Our paper showing how a transposable element (TE) insertion can cause developmental phenotypes is now published @natgenet.nature.com 🧬🦠🐁
Below is a brief description of the major findings. Check the full version of the paper for more details: www.nature.com/articles/s41588-025-02248-5

Calling all aspiring Postdocs! One extra week to apply to join our exciting HFSP-funded project to uncover how chromatin moves to function.

Deadline July 15th.

www.mdc-berlin.de/career/jobs/...

How do non-coding variants in enhancers lead to disease? Happy to share our recent work, led by @ewholling.bsky.social, in which we discovered that poised chromatin sensitizes enhancers to aberrant activation by non-coding mutations, contributing to disease. www.biorxiv.org/content/10.1... 1/

Non-canonical enhancers control gene expression and cell fate in human pluripotent stem cells Enhancers are key gene regulatory elements that ensure the precise spatiotemporal execution of developmental gene expression programmes. However recent findings indicate that approaches to identify en...

Delighted & excited to share our latest preprint on non-canonical enhancers in human pluripotent stem cells, the result of a fantastic and fun collaboration with @guenesdoganlab.bsky.social‬:
www.biorxiv.org/content/10.1...

🧵 below

Conservation of regulatory elements with highly diverged sequences across large evolutionary distances Nature Genetics - Combining functional genomic data from mouse and chicken with a synteny-based strategy identifies positionally conserved cis-regulatory elements in the absence of direct sequence...

How to find Evolutionary Conserved Enhancers in 2025? 🐣-🐭
Check out our paper - fresh off the press!!!
We find widespread functional conservation of enhancers in absence of sequence homology
Including: a bioinformatic tool to map sequence-diverged enhancers!
rdcu.be/enVDN
github.com/tobiaszehnde...

We're thrilled to continue our deep dive into how chromatin mechanics govern how our genomes function with our A-team @andersshansen.bsky.social @Davide Michieletto, and @Sandra Tenreiro.

A huge thanks to the @dfg.de and @hfspo.bsky.social for supporting us.

Stay tuned! PhDs/Postdocs coming soon!

portrait of a man

@drmrobson.bsky.social has won two grants from @dfg.de & @hfspo.bsky.social totaling over €2 million. He and his lab now work to decode the mechanics of #chromatin, hoping to finally define its physical state and better understand how it governs gene regulation
www.mdc-berlin.de/news/news/mi...

Thanks also to the @stemundi.bsky.social lab where this work started and the Robson lab where it was finished! Last, my amazing supervisor @drmrobson.bsky.social who devised the inducible DamID mouse and spearheaded the project!

Huge thanks to the Wunder-Kinder @imguerreiro.bsky.social, Samy & @jopkind.bsky.social without whom this project wouldn’t have happened, and to Alex and Andrea from @marionicodemi.bsky.social lab for modeling.

3️⃣ So what links this pre-activation repositioning to multipotency? We find it's closely tied to increased chromatin accessibility at sites bound by key limb transcription factors. This includes several factors shown to act together via a “coordinator motif” doi.org/10.1016/j.ce...

2️⃣ But not only genes reposition. Genes escape the periphery together with the surrounding enhancers and TADs that control their expression. Using polymer modeling & mutants, we show that CTCF boundaries and 3D chromatin topology prevent this repositioning from spreading to neighboring regions.

1️⃣ At the start of limb formation, hundreds of genes move away from the repressive nuclear periphery in multipotent progenitors. Amazingly, this repositioning can precede gene activation by up to four developmental days (E9.5 -> E13.5), suggesting it is a key priming step for multipotency!

Developmental genes have really precise expression in time and space and so must spend most of their time inactive. So how and when do they "wake up" to perform their function? Leveraging scDam&T-seq in embryonic limb development, we uncover three exciting new insights:

Reconfiguration of genome-lamina interactions marks the commissioning of limb cell-fates Diverse forms of heterochromatin block inappropriate transcription and safeguard differentiation and cell identity. Yet, how and when heterochromatin is reconfigured to facilitate changes in cell-fate...

🚨 Preprint 🚨
Ever wondered how cells prepare their genomes to enable new cell-fates? In this team up with the Kind lab, we show that genes are repositioned in the nucleus to get ready for future activation and tissue formation. Read 🧵👇 to find out how and when this happens!

doi.org/10.1101/2025...

Chromatin loops are an ancestral hallmark of the animal regulatory genome - Nature The physical organization of the genome in non-bilaterian animals and their closest unicellular relatives is characterized; comparative analysis shows chromatin looping is a conserved feature of ...

I’m very excited to share our work on the early evolution of animal regulatory genome architecture - the main project of my postdoc, carried out across two wonderful and inspirational labs of @arnausebe.bsky.social and @mamartirenom.bsky.social. www.nature.com/articles/s41...

I am elated to share that our manuscript describing Variant-EFFECTS, a high-throughput technology we developed to precisely and quantitatively measure the effects of CRISPR-mediated edits on gene expression, is now published at @cellpress.bsky.social: authors.elsevier.com/c/1kxgiL7PXu...

Grateful to my wonderful collaborators worldwide:
Yuko Sato, Xingchi Yan, Simon Ulrich, @watanyatra.bsky.social, Lothar Schermelleh, Hiroshi Kimura, IrinaSolovei & my supervisor @drmrobson.bsky.social. Thank you for your hard work & support throughout! 🌍🙏

Is your rim staining real, or Ab-trapping? Solutions:
✅ Increase incubation time
✅ Tissue sections (antigen retrieval)
✅ Use lower-affinity antibodies/nanobodies
✅ Check cell-to-cell expression: rims only in high-expression cells = likely artifact

This artifact can impact any assay that relies on antibody diffusion, such as classic fluorescence microscopy, but also new-generation genomics techniques, such as CUT&Tag and CUT&RUN - SO WATCH OUT. See falsely peripheral H3K9Me2 Cut&Tag in mouse rod cells 👇

Ab-trapping occurs when antibodies fail to penetrate due to:
1️⃣ High epitope abundance
2️⃣ High antibody affinity
3️⃣ Low diffusion rate
Any one factor is enough! Potentially affects many antibody–epitope pairs under the right conditions. Examples 👇

Ab-trapping - a peripheral staining artifact in antibody-based microscopy and genomics Antibodies (Ab) are essential for detecting specific epitopes in microscopy and genomics, but can produce artifacts leading to erroneous interpretations. Here, we characterize a novel artifact, Ab-tra...

🚨 Preprint alert 🚨
Excited to share our work on "Ab-trapping," an antibody artifact causing misleading peripheral ("rim") staining in imaging & genomics (IF, CUT&Tag, CUT&RUN). Antibodies fail to penetrate structures, accumulating at the periphery. A 🧵👇
doi.org/10.1101/2025...

Grateful to my wonderful collaborators worldwide:
Y. Sato, X. Yan, S. Urlich, @watanyatra.bsky.social, L. Schermelleh, @gfudenberg.bsky.social, H. Kimura, I. Solovei & my supervisor @mikerobson.bsky.social. Thanks for your hard work & support! 🤝🌍

Is your rim staining real, or Ab-trapping? Solutions:
✅ Increase incubation time
✅ Tissue sections (antigen retrieval)
✅ Use lower-affinity antibodies/nanobodies
✅ Check cell-to-cell expression: rims only in high-expression cells = likely artifact

This artifact can impact any assay that relies on antibody diffusion, such as classic fluorescence microscopy, but also new-generation genomics techniques, such as CUT&Tag and CUT&RUN - SO WATCH OUT. See falsely peripheral H3K9Me2 Cut&Tag in mouse rod cells 👇

Ab-trapping occurs when antibodies fail to penetrate due to:
1️⃣ High epitope abundance
2️⃣ High antibody affinity
3️⃣ Low diffusion rate
Any one factor is enough! Potentially affects many antibody–epitope pairs under the right conditions. Examples 👇