Gerlich Lab

Gerlich Lab

@gerlichlab.bsky.social

We study how genomes change shape to make biology work through genomics, imaging, reconstitution, & computation. Lab website: oeaw.ac.at/imba/research/daniel-gerlich Located at @imbavienna.bsky.social, part of @viennabiocenter.bsky.social

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Our latest paper is out in @embojournal.org! Chromatin compaction is a hallmark of apoptosis, but the mechanism & function of this process was unclear. We show apoptotic compaction is required to prevent fragmented DNA from spreading beyond the dying cell, and is driven by histone deacetylation.

The EMBO Journal@embojournal.org

How does DNA remain confined to dying cells despite its fragmentation? @mfdspicer.bsky.social @rcollepardo.bsky.social @gerlichlab.bsky.social et al show histone deacetylation compacts apoptotic chromatin, preventing it from entering apoptotic extracellular vesicles link.springer.com/article/10.1...

To understand how histone deacetylation drives compaction in apoptosis & living cells, we used synthetic nanobodies to direct charge to the nucleosome surface. Our charged nanobodies drove compaction & decompaction in cells, showing nucleosome electrostatics alone can determine chromatin density.

At Falling Walls Lab Vienna, 10 early-career researchers had just 3 minutes each to explain a complex research idea clearly and convincingly. Neos was selected among the top 3 pitches of the competition. Bravo! 🎉👏 More about the competition and finalists here (in German): lbg.ac.at/news/junge-t...

lbg.ac.atJunge Talente, große Ideen: Die Finalist:innen des Falling Walls Lab Vienna 2026 stehen fest – Ludwig Boltzmann GesellschaftForschung, die beim Menschen ankommt.

Congratulations @golobor.bsky.social and the whole team! Always great collaborating on some very cool science 🧬👏

Anton Goloborodko@golobor.bsky.social

1/ out in @science.org! We found a new asymmetry in large-scale chromosome structure: sister chromatids are shifted by hundreds of kb in the 5′→3′ direction of their inherited strands! A close collaboration w/ @gerlichlab.bsky.social , led by @flaviacorsi.bsky.social www.science.org/doi/10.1126/...

Gerlich Lab reposted

Replying to @golobor.bsky.social

Thomas Steinacker from @gerlichlab.bsky.social found a way to verify this using optical microscopy and RASER-FISH. He developed strand-specific probes and hybridized them to individual sisters, thus measuring distances between sister loci and visualizing the shift. 8/

Our paper is out in The EMBO Journal @embojournal.org! 🎉 We show how replicated chromosomes can maintain sister chromatid cohesion while still allowing dynamic loop folding within nested hierarchy of TADs. Check it out below 👇 1/2

The EMBO Journal@embojournal.org

How do replicated #chromosomes coordinate sister chromatid cohesion with dynamic loop folding? @gerlichlab.bsky.social and collaborators identify cohesion zones within the nested TAD hierarchy as organizational principle reconciling these two #cohesin functions link.springer.com/article/10.1...

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The consortium was also about community: BBQs, sushi nights, and plenty of time together outside the lab 🍣🔥. Huge thanks to the Isenberg family for supporting the consortium, both this year and over the years. 3/4

Last month’s Lab Retreat at Gustav Ammerer’s castle 🏰🌿 Hiking, cooking together, personality tests, TED-style talks, and a very intense round of Blood on the Clocktower. A lovely few days of science, reflection, games, food, and getting to know the lab beyond work and the bench.

Congratulations again, Max! 🎉 We’re so proud of you and grateful to have had you in the lab. Wishing you all the best for the exciting next chapter! 👏

Max Spicer@mfdspicer.bsky.social

Chuffed to have defended my PhD thesis! Big thanks to @danielgerlich.bsky.social for all his support and guidance; and to the wonderful @gerlichlab.bsky.social, @imbavienna.bsky.social & @viennabiocenter.bsky.social for being an incredible scientific home these past few years. On to the next :)

The Gerlich lab recently attended the International Symposium on Chromosome Dynamics: from Structure to Cellular Function in Awaji, Japan 🇯🇵 A really nice chance to share our work, exchange ideas, and catch up with the chromosome dynamics community. 1/3

Max’s work showed that histone tail deacetylation drives chromatin compaction during apoptosis, helping prevent DNA release into apoptotic extracellular vesicles. This work was also a collaboration with @rcollepardo.bsky.social and the Rosen labs. More in our thread here: 2/2

Gerlich Lab@gerlichlab.bsky.social

1/New preprint just dropped! 🔥🔥 We investigate how the genome is destroyed in apoptotic cells in a way that prevents DNA fragments from spreading beyond the dying cell 🧬⚰ Done here at @imbavienna.bsky.social & in the super @rcollepardo.bsky.social & Rosen labs: www.biorxiv.org/content/10.6...

Welcome to the Gerlich Lab, Valerio! 🎉 We’re excited to have you on board and look forward to the great science ahead together. 🧬

Valerio Sorichetti@vsorichetti.bsky.social

I'm happy to share that I have started a new position in the Gerlich Lab (@gerlichlab.bsky.social) at IMBA (@imbavienna.bsky.social) as Senior Bioinformatician. Looking forward to contributing to the great science developed in the group! 😊🧬

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This creates a nested hierarchy: top-level boundaries act as discrete "cohesion zones" linking sisters for repair, while smaller, nested domains loop independently for gene regulation. 3/6

Using sister-chromatid-sensitive Hi-C & ChIP-seq, we found these two functions are spatially partitioned! Total cohesin (RAD21) anchors across all TAD boundaries, but the specific cohesive subset (Sororin) is enriched primarily at high-level boundaries. 2/6

Congratulations to Caelan on completing their PhD! 🎉 Last week, they defended their thesis, “Unravelling the Surface Localisation of Centromeres on Vertebrate Chromosomes in Mitosis.” The lab is very proud of you, Caelan! 👏 1/2

Caelan’s work is also part of a recent preprint from a collaboration between the Rosen, Redding, Collepardo-Guevara, and Gerlich labs, showing that electrostatic repulsion positions centromeres at the chromosome surface during mitosis. More in our thread here: 2/2

Gerlich Lab@gerlichlab.bsky.social

1/ New preprint alert! In collaboration between the Rosen, Redding, Collepardo-Guevara & Gerlich labs, we uncover a surprising principle of chromosome organisation: electrostatic repulsion positions centromeres at the chromosome surface during mitosis. 🔗 doi.org/10.1101/2025...

Last week, the Gerlich lab went to Prein an der Rax for a writing retreat, or as we liked to call it, a “storython” ✍️🏔️ Led by Iain Patten, it was a chance to step away from day-to-day experiments and focus on building clearer, more coherent stories around our research. 1/4

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The retreat included group discussions, focused thinking and writing time, amazing food, evenings by the bonfire, and a beautiful setting surrounded by nature 🌿🐦 A really nice mix of science, reflection, and time together. 3/4

Last week, the Gerlich lab went to Prein an der Rax for a writing retreat, or as we liked to call it, a “storython” ✍️🏔️ Led by Iain Patten, it was a chance to step away from day-to-day experiments and focus on building clearer, more coherent stories around our research. 1/4

The goal was to think beyond individual results: What is the bigger question? What is the core message? Why does it matter? And how do the different pieces of a project come together into a compelling scientific story? 💬📝 2/4

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9/Our results show apoptotic chromatin compaction, driven by histone deacetylation, sequesters DNA fragments produced during genome destruction. Synthetic perturbations suggest charge alone is enough to induce compaction, which may help us to better understand and alter chromatin in living cells

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7/Expression of the positively charged nanobody in live cells caused chromatin hypercompaction, while the negatively charged nanobody induced a homogenous phenotype reminiscent of HDAC inhibition. In vitro & in silico, nanobody addition alone caused similar changes in chromatin structure

8/These charge manipulations also affected chromatin compaction in apoptotic cells: In the presence of positive nanobodies, chromatin compacted despite blocked histone deacetylation; while the negative nanobody caused the same decompaction phenotype as HDAC inhibition

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5/We wondered if compaction might also prevent DNA from entering apoptotic extracellular vesicles, which are shed from the plasma membrane of the dying cell. ApoEVs are usually devoid of DNA, but became filled with chromatin fragments when we inhibited histone deacetylation

6/Histone deacetylation leads to chromatin compaction in living & dying cells, potentially by a direct electrostatic effect. To understand the role of charge in apoptotic chromatin, we created nucleosome-binding nanobodies fused to GFP mutants of opposing charge

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3/Chromatin is compacted in apoptosis, might this sequester fragments? Histone deacetylation, which drives compaction in living cells, has been observed in apoptosis, but a role in apoptotic compaction was unknown. We inhibited apoptotic deacetylation which resulted in drastic chromatin decompaction

4/This decompacted phenotype was less dense than interphase nuclei & resembled chromatin fragments mixing with cytosol. To test this, we blocked deacetylation in cells lacking the apoptotic endonuclease CAD. Without fragmentation, hyperacetylation induced chromosome swelling but no dispersion of DNA

2/Apoptosis happens billions of times each day in the human body, during which the genome is destroyed by fragmentation. Despite being cut into short stretches, chromatin remains sequestered within a single cell corpse. How is fragmented DNA prevented from escaping the dying cell?