Karin Prummel

This 🐍 venom made so many cool multi-day live imaging sessions possible 🔬🐟🩸 @chrmosimann.bsky.social @huiskenlab.bsky.social @daetwylerstephan.bsky.social

An inflammatory T-cell-stromal axis contributes to hematopoietic stem/progenitor cell failure and clonal evolution in human myelodysplastic syndrome - Nature Communications Mechanisms of clonal evolution in myeloid neoplasms remain incompletely understood. Darwinian theory predicts that the (micro)environment of clone-propagating stem cells may contribute to clonal selec...

Lastly, a shout-out to Marc Raaijmakers’ team at
@erasmusmc.bsky.social 🎉📢 whose complementary work led by Lanpeng Chen and Yujie Bian revealed similar inflammatory bone marrow remodeling in MDS and made a link to leukemic evolution. A story that unfolded in parallel! ✏️
shorturl.at/4G8Yr

Huge thanks to my fellow co–first authors Kevin and Maksim: together we pushed this project forward. 💪 Grateful to Judith and Borhane for support 🙏 and all collaborators @embl.org @biomedizin.unibas.ch @unimainz.bsky.social @tudresden.bsky.social @dkfz.bsky.social @trowbridgelab.bsky.social @ki.se

🎯 Inflammation and niche remodelling are hallmarks in both CHIP to MDS, underscoring the role of the microenvironment in early myeloid disease. Targeting this stromal-immune remodelling could open new interception strategies.

In co-culture experiments 🧫, we showed that healthy & CHIP HSPCs engaged with stromal cells to receive support 🩸🫂(e.g., CXCL12), but MDS HSPCs failed to do so. MDS blasts (!) even triggered an inflammatory program in stromal cells.

SpliceUp: Predicting SF3B1 mutations in individual cells via aberrant splice site activation from scRNA-seq data Myeloid neoplasms (MN) are clonal heterogeneous disorders initiated by somatic driver mutations in hematopoietic stem and progenitor cells (HSPCs). Among the most common are mutations in RNA splicing ...

Together with collaborators from @ki.se, we developed and applied SpliceUp, a pipeline for detecting aberrant splicing from scRNA-seq (shorturl.at/d8Evh), and could detect splice factor (SF3B1) mutated MDS cells. We showed that these mutated HSPCs in MDS are not directly driving inflammation.

On the immune side 🧪: we found IFN-responsive T cells enriched in MDS that preferentially interact with iMSCs, hinting at a stromal-immune axis of bone marrow niche inflammation. An inflammatory feedback loop?

Key finding: we identified a novel population of “inflammatory mesenchymal stromal cells” (iMSCs) that appear in asymptomatic and already low-VAF CHIP and expand further in MDS, while healthy CXCL12+ adipogenic stromal cells decline in the bone marrow. 🧬🔬

We studied human bone marrow samples from 84 donors (age-matched healthy controls, CHIP carriers, and early MDS patients) using single-cell RNA-seq, imaging, flow cytometry, and functional co-culture assays. 🧫

The scale of human stromal niche profiling is what makes this study special! 🦴🩸🧬🔬

🚨 Excited to share our paper 📢 @natcomms.nature.com
We reveal how inflammation reshapes the human #bonemarrow niche 🦴, home of 🩸 stem cells, in the context of #clonalhematopoiesis and #myelodysplasia

An amazing journey with fantastic colleagues and collaborators, thank you all!

shorturl.at/ad0st

Huge thanks to my fellow co–first authors Kevin and Maksim: together we pushed this project forward. 💪 Grateful to Judith and Borhane for support 🙏 and all collaborators @embl.org @biomedizin.unibas.ch
@unimainz.bsky.social @tudresden.bsky.social @dkfz.bsky.social @trowbridgelab.bsky.social @ki.se

🎯 Inflammation and niche remodelling are hallmarks in both CHIP to MDS, underscoring the role of the microenvironment in early myeloid disease. Targeting this stromal-immune remodelling could open new interception strategies.

In co-culture experiments 🧫, we showed that healthy & CHIP HSPCs engaged with stromal cells to receive support 🩸🫂(e.g., CXCL12), but MDS HSPCs failed to do so. MDS blasts (!) even triggered an inflammatory program in stromal cells.

SpliceUp: Predicting SF3B1 mutations in individual cells via aberrant splice site activation from scRNA-seq data Myeloid neoplasms (MN) are clonal heterogeneous disorders initiated by somatic driver mutations in hematopoietic stem and progenitor cells (HSPCs). Among the most common are mutations in RNA splicing ...

Together with collaborators from @ki.se, we developed and applied SpliceUp, a pipeline for detecting aberrant splicing from scRNA-seq (shorturl.at/d8Evh), and could detect splice factor (SF3B1) mutated MDS cells. We showed that these mutated HSPCs in MDS are not directly driving inflammation.

On the immune side 🧪: we found IFN-responsive T cells enriched in MDS that preferentially interact with iMSCs, hinting at a stromal-immune axis of bone marrow niche inflammation. An inflammatory feedback loop?

Key finding: we identified a novel population of “inflammatory mesenchymal stromal cells” (iMSCs) that appear in asymptomatic and already low-VAF CHIP and expand further in MDS, while healthy CXCL12+ adipogenic stromal cells decline in the bone marrow. 🧬🔬

We studied human bone marrow samples from 84 donors (age-matched healthy controls, CHIP carriers, and early MDS patients) using single-cell RNA-seq, imaging, flow cytometry, and functional co-culture assays. 🧫

The scale of human stromal niche profiling is what makes this study special! 🦴🩸🧬🔬

Sonoepigenetic Modification Mechanoprimes Early Osteogenic Commitment in Mesenchymal Stem Cells Cells effectively balance and integrate numerous pathways to adapt to external signals in an attempt to regain homeostasis, although the complex nuclear mechanotransduction mechanism through which thi...

As we wait for the final version in the journal, I leave here the last version that we uploaded on bioarchive.
I hope you like it!

www.biorxiv.org/content/10.1...

Join EMBL as a research group leader in AI in biology. EMBL AI is our new initiative aiming to exploit the full potential of ML/AI-based approaches to advance our understanding of the most complex system in the known universe - life on Earth.
embl.wd103.myworkdayjobs.com/en-US/EMBL/j...
(1/3)

We are all super happy and proud to see our work on the function and evolution of the #cephalic #furrow published in @nature.com. Let me say a few things about the background and history of this work on the #Evolution_of_Morphogenesis (1/12)

Research Technician We are looking for a highly motivated research technician to join the Zaugg group at EMBL Heidelberg, an interdisciplinary team of experimental and computational scientists. Our research combines larg...

We are searching for a research technician in our group at EMBL Heidelberg! 🧫🧬🔬

For more details, see the ad. Please reach out in case of any questions.

The position is ideally filled by October 1.

embl.wd103.myworkdayjobs.com/en-US/EMBL/j...

🚨 @dkfz.bsky.social Postdoctoral Fellowships 2025 — Postdoc opening (Mall Lab)
Work at the interface of neurodevelopment, epigenetic repression & cancer neuroscience.
Apply: jobs.dkfz.de/en/jobs/1679...
#Postdoc #Plasticity #Neurodegeneration #CancerNeuroscience

Looking for a #postdoc opportunity? Funded positions available @cuanschutz.bsky.social to advance our #zebrafish transgenesis tools - and to look into developmental origins of congenital disease!
#devbio

Excited to share our latest paper @natmethods.nature.com
We present a high-throughput framework to map cellular interactions at ultra-high scale – broadly applicable from whole-organism immune response mapping to personalized therapy response prediction (1/4).
www.nature.com/articles/s41...

Group Leader - Genome Biology Unit Are you ready to lead groundbreaking research in Genome Biology? Join us at EMBL! We are seeking a motivated scientist to lead an independent research group addressing exciting and original biological...

To all post-docs: The Genome Biology dept ‪@embl.org
has an Independent faculty position. Fantastic place to set up your lab –great package: core funding, fantastic Ph.D. students, cutting edge core facilities & great colleagues. Closing date Sept 19th
embl.wd103.myworkdayjobs.com/en-US/EMBL/j...

Congratulations Maria with this great story! I'm happy that your visit to our groups at EMBL was so productive and we could support you with the single-cell multiomics experiments. 🧬🧫🧠

Thrilled to share the story stemming from my PhD!
We used mESC neural differentiation, genome editing and bulk & single-cell approaches to uncover how ZIC2 controls early neural fate by playing a dual and sequential regulatory role as a promiscous pioneer and a selective lineage-specific activator.

🥁 New article 📢: #Mechanobiology of #development during #Drosophila #gastrulation using #Brillouin microscopy, now in @natcomms.nature.com : rdcu.be/ev6ZX
Collab. w/ @Prevedel_Lab @embl.org , Maria Leptin @marialep.bsky.social, @abhisha-thayambath.bsky.social, Julio Belmonte @ncstate.bsky.social

Single-cell ultra-high-throughput multiplexed chromatin and RNA profiling reveals gene regulatory dynamics - Nature Methods This work presents SUM-seq, an ultra-high-throughput method for co-profiling chromatin accessibility and gene expression in single nuclei across multiplexed samples, advancing the study of gene regula...

SUM-seq: New single-cell method by @biomedizin.unibas.ch , @embl.org , @au.dk ‬‬ and Tampere university enables large-scale analysis of gene activity & DNA accessibility across millions of cells.
Congrats Prof. Zaugg & collaborators!‬‬‬‬‬‬

🔗 www.nature.com/articles/s41...

Looking for an ultra-high-throughput single-cell RNA+ATAC method? 🎆

Check out our SUM-seq method, now officially out! 🧬

Showcased on macrophages, T cells, and iPSC-derived embryoid bodies; more cell types and tissues to come! 🧫

Reach out for the detailed protocol! 📝 ✨