10/Enormous congratulations to all contributors, including first author @mfdspicer.bsky.social on his PhD work here at @imbavienna.bsky.social @viennabiocenter.bsky.social 🎓🎉
Read the full pre-print here: www.biorxiv.org/content/10.6...
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
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
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
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
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
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
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
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?
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...
The Vienna BioCenter Summer School 2026 call is now open for talented undergrads, it's a great for those interested in graduate study in the life sciences. Daniel Gerlich from Institute of Molecular Biotechnology is recruiting! Please share
https://training.vbc.ac.at/summer-school/
And don’t miss the insightful Science Perspective by Jiazhi Hu, placing both studies in context:
🔗 www.science.org/doi/10.1126/...
Also, check out the related work by @albertomarin.bsky.social from the Ha and Scully labs, who approached homology search and repair from a complementary angle:
🔗 www.science.org/doi/10.1126/...
A big thank you to everyone at @imbavienna.bsky.social and across the @viennabiocenter.bsky.social for their support throughout this project: from the outstanding facilities to the collaborative campus environment that made this work possible.
Excited to share our latest fully in-house paper! 🎉
We show how cohesin integrates loop extrusion with sister tethering to guide the homology search during DNA repair.
Huge congratulations to all authors, and to @fedeteloni.bsky.social for leading this work 👏
We’re excited to see his next steps!
🚨 New Science paper from the Gerlich lab!
The team shows how cohesin helps broken DNA find the right template: by opening local DNA loops to shrink the search area and by keeping the damaged strand close to its sister copy: science.org/doi/10.1126/science.adw0566
“Maximilian Spicer holding the Best Poster Prize certificate at the 2nd Spatial Genome Organization Conference.”
Huge congratulations to @mfdspicer.bsky.social, PhD student in our lab, for winning the Best Poster Prize at the 2nd Spatial Genome Organization Conference! 🎉
A proud moment for the lab and well-deserved recognition for his creativity and dedication. 👏
@fusionconf.bsky.social #SGO25
13/ Proud to share this work led by co-first authors Caelan Bell, Lifeng Chen & Julia Maristany, with contributions from many colleagues across the Rosen, Redding, Collepardo-Guevara & Gerlich labs.
Full story here 👇
🔗 doi.org/10.1101/2025...
12/ In short:
Centromere positioning is not hardwired by folding patterns.
It emerges from physics — specifically, charge-based repulsion.
11/ This modular principle likely extends beyond mitosis — shaping genome organisation in interphase, and offering routes for synthetic control of genome positioning.
10/ Conceptually, it’s like amphiphiles at oil–water interfaces: attraction inside, repulsion outside → stable layering.
9/ Together these findings reveal a general principle:
Centromere layering emerges from electrostatic polarity — a charge-based asymmetry that repels certain domains outward while the rest integrate inward.
8/ We built a synthetic system: TetR fused to a negatively charged GFP.
When tethered to chromatin, this construct drove loci to the surface — in vitro and in cells.
7/ Adding pure DNA segments to nucleosome arrays was enough to push them outward, in cryoET of chromatin condensates and MD simulations.
👉 Negative charge induces surface targeting.
6/ In vitro chromatin condensates and molecular dynamics simulations showed why.
CENP-B’s acidic domain was sufficient to drive nucleosome arrays to the condensate periphery.
5/ When we depleted kinetochores via CENP-C, centromeres shifted inward.
Knocking out CENP-B further reduced surface localisation.
👉 Kinetochores + CENP-B cooperate to position centromeres at the surface.
4/ Even after condensin depletion and spindle depolymerisation, CENP-A centromere cores still localised at the chromosome periphery.
👉 Surface localisation is independent of loops & spindles.
3/ Prevailing models suggested centromeres are placed at the surface by specific chromatin loop architectures. But our work shows this positioning emerges instead from electrostatic repulsion.
2/ Why does this matter?
Centromeres must locate at the chromosome surface to allow kinetochores to attach spindle microtubules. If buried inside, microtubules can’t reach kinetochores to segregate chromosomes faithfully.
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...
