iiinova — where your digital self keeps evolving

Always grateful to be back in Woods Hole and at MBL—a very special place to do science and spend time by the sea. 🌊🌈 4/4

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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

We set up a shared lab in the Lillie Laboratory at @mblscience.bsky.social, where working side by side made it easy to move between discussions, troubleshooting, and experiments. 🔬💬 2/4

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Gerlich Lab @gerlichlab.bsky.social · 15/07/2026

That’s a wrap on this year’s Chromatin Consortium in Woods Hole! 🧬 The @danielgerlich.bsky.social , @rcollepardo.bsky.social , @vram142.bsky.social, Gibson, and Rosen labs came together to exchange ideas, run experiments, and explore chromatin organisation from different angles. 1/4

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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.

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Gerlich Lab @gerlichlab.bsky.social · 09/06/2026

Takuya, Mustafa @mualaabo.bsky.social, and Dmitry @dmitrymyl.bsky.social also presented their projects during the poster session. Great to see the lab so well represented and to have many inspiring discussions throughout the meeting. 👏 3/3

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Gerlich Lab @gerlichlab.bsky.social · 09/06/2026

Daniel @danielgerlich.bsky.social presented Caelan’s work in a talk titled “An electrostatic repulsion model of centromere organization,” highlighting how electrostatic repulsion helps position centromeres at the chromosome surface during mitosis. 2/3

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Gerlich Lab @gerlichlab.bsky.social · 09/06/2026

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

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Gerlich Lab @gerlichlab.bsky.social · 29/05/2026

A very well-deserved pop for a big milestone 🥂🎉

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Gerlich Lab @gerlichlab.bsky.social · 29/05/2026

Congratulations to Max @mfdspicer.bsky.social on completing his PhD! 🎉 Yesterday, he successfully defended his thesis, “Electrostatic control of apoptotic chromatin compaction.” The lab is very proud of you, Max! 👏 1/2

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Gerlich Lab @gerlichlab.bsky.social · 06/05/2026

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

Alt text for the pic: Model depicting sister chromatid organization as defined by TAD hierarchy.

Gerlich Lab @gerlichlab.bsky.social · 06/05/2026

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

Left: average profiles of Sororin (upper panel) and RAD21 (lower panel) ChIP-Seq signal (1 kb resolution) at ±100 kb regions centered at high-, mid- and low-level boundaries. Right: average maps of trans sister (upper row) and cis sister (lower row) scsHi-C contacts (10 kb resolution) at ±1 Mb regions centered at high-, mid-, and low-level boundaries, normalized to genome-wide expected contact frequencies.

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Gerlich Lab @gerlichlab.bsky.social · 27/04/2026

A well-deserved celebration for a big milestone 🥂🎉

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Gerlich Lab @gerlichlab.bsky.social · 27/04/2026

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

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Gerlich Lab @gerlichlab.bsky.social · 20/04/2026

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

Gerlich Lab @gerlichlab.bsky.social · 20/04/2026

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

Gerlich Lab @gerlichlab.bsky.social · 20/04/2026

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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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

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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

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?

Gerlich Lab @gerlichlab.bsky.social · 11/11/2025

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

“Maximilian Spicer holding the Best Poster Prize certificate at the 2nd Spatial Genome Organization Conference.”

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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.

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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.

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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.

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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.

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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.