Maximilian Billmann @maxbillmann
Asst Prof @UniBonn @UniklinikBonn | dataScience, ML, funGenomics, CRISPRscreens | Postdoc @UMNComputerSci @DonnellyCentre | PhD @Michael_Boutros @wolfgangkhuber Bonn, Germany Joined August 2015-
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As I have pointed out many times publicly, single cell foundation model performance will scale with the number of perturbations, not the number of cells. We barely have ~100k perturbations in the public domain and it is reasonable to expect we need millions to truly go OOD.
Balancing off-target and on-target considerations for optimized CRISPR-Cas9 knockout library design dlvr.it/TSXnjP
Buffering of gene dosage response curves for human complex traits dlvr.it/TSQXBN
We’re hiring in Bonn! 📢 The University of Bonn seeks applications for a W2 Professorship in Mathematics in Medical Sciences. 📅 Deadline: July 5, 2026 uni-bonn.de/de/universitae…
🚨Publication alert🚨 My first-author PhD paper is out today in Nature Genetics nature.com/articles/s4158… Tumors aren’t one entity — they’re made of coexisting cell states with distinct vulnerabilities. We show that targeting complementary states simultaneously in DMG is key.
CRISPR activation screens map the genomic landscape of cancer glycome remodeling dlvr.it/TRxwJR
Great to the see the flurry of single gene knockdown Perturb-seq like atlases from cell-lines, mouse brain etc over the last few days. These are undoubtedly very valuable datasets. I just want to re-iterate a few other very important expt. design considerations 1/
One should have expected such comparisons in any early virtual cell paper...
How much value will virtual cell models add compared to querying the training data with DeSeq2 and Pearson correlations? Have people seen virtual cell demos with better enrichment of positive controls than Fig. 1?
Proud of my colleagues for this remarkable work. Congrats Axel!
🆕@Nature Genome sequencing of >800,000 people finds Epstein-Barr virus reads and their association with other autoimmune diseases besides multiple sclerosis, including type 1 diabetes, inflammatory bowel disease, and hypothyroidism nature.com/articles/s4158…
Happy to share that my postdoctoral work is now out in @ScienceMagazine. We show that the RNA-programmable bridge recombinase ISCro4 can insert, delete, or invert multi-kilobase DNA fragments at defined genomic sites in human cells. Study link: science.org/doi/10.1126/sc… CRISPR-Cas has transformed genome editing, but many diseases involve diverse patient-specific mutations within the same gene. A mutation-agnostic alternative is to insert a healthy gene copy at a defined genomic locus, but gene-sized, site-specific insertions remain a major challenge. Main findings of our work: (1) ISCro4 is highly active in human cells and can be delivered by plasmid or all-RNA formats (2) Proof-of-concept programmable multi-kb insertions, deletions, and inversions (3) Structural insights into the basis of enhanced ISCro4 activity (4) Specificity and off-target characterisation (5) A framework to support future development and adoption of bridge recombinases The work was made possible through a close collaboration between the Jinek Lab, @schwanklab, and @jcornlab. I am deeply grateful to all of my co-authors for the team spirit, hard work, and dedication that went into this publication: @talasandris, Javier Fernández Carrera, @nicopmat, Lilly van de Venn, Charles Yeh, @p_kulcsar, @marquark, @YanikWeber, @SaskiaGerecke, Isabelle Harvey-Seutcheu, Dominic Mailänder, @MorPfl, and @ChrisChanez89. Special thanks to my supervisor, Prof. Martin Jinek, for his outstanding mentorship, and to Prof. Gerald Schwank and Prof. Jacob Corn for their generous support throughout. Finally, I would like to thank everyone in the Jinek lab for creating a supportive work environment, and @EMBO for funding my postdoctoral work. In parallel, independent work led by @ntperry13, @SKonermann and @pdhsu also reported ISCro4 activity in human cells, reinforcing the robustness and momentum of this direction. Please reach out if you would like to test the system or discuss potential applications. Relevant plasmids are now available via @Addgene.
🚀 Excited to share new paper in Nature Genetics: Human Retina Cell Atlas (HRCA) with ~4M cells, >130 retinal cell types, deep scRNA/ATAC integration. Enables cross-species comparisons & GWAS cell-type enrichment. Huge thanks to Ignacio Ibarra & Chen lab. nature.com/articles/s4158…
Our paper is published in @CellReports! We apply a multi-omic framework to analyze nearly 2,000 noncoding variants at risk loci for age-related macular degeneration and nominate 59 variants as pathogenic. A great collab w/ @Jiaying_Gia @suragnair @anshulkundaje and @HowardYChang!
Single-cell multiome and enhancer connectome of human retinal pigment epithelium and choroid nominate causal variants in macular degeneration dlvr.it/TQSksf
@thenormanlab Much appreciated! There is so much to be screened. I look forward to complete reading your preprint.
Amazing new data set by @thenormanlab, congrats! Not sure about the 'biggest GI map in human cells' though. I guess it depends how you count, but we covered quite a number of gene pairs too: doi: 10.1101/2025.06.30.662193
Using PORTAL with an AP-1 reporter, we measured 665,856 pairwise perturbations across 612 genes and 46 million clonal lineages. To our knowledge, this is the largest exhaustively measured GI map in human cells, and the first at this scale with a non-fitness phenotype.
In my excitement I forgot to actually link the preprint! biorxiv.org/content/10.648…
🚀 Announcing the Official @OpenTargets MCP! We've partnered with @AnthropicAI to provide AI with seamless access to high-quality genetics and target-discovery data. Open for the entire community to accelerate therapeutic development blog.opentargets.org/official-open-…
Why define conditions, donors or even *tasks* when we can just use cells themselves to guide model output Presenting Stack, in-context learning using just cells! Use cell context -> enhance its embedding Engineer cell context ->modify its state Led by the brilliant @Mingze7316
Together with Emma Dann, we are thrilled to present a massive new Perturb-seq atlas of 22M primary CD4+ T cells, from 4 donors, across 3 timepoints – the result of a decade-long collaboration between the Marson (@MarsonLab) and Pritchard (@jkpritch) labs. 🧵👇
Impressive effort
Pooled screening of secreted factors (cytokines, growth factors) is difficult due to paracrine cross-talk. By genetically tethering ligands to the cell surface to enforce obligate autocrine signaling, OASIS enabled a pooled screen of the entire human ligandome (~770 factors) in
An Analysis compares the performance of 27 single-cell perturbation response prediction methods under comprehensive test conditions. nature.com/articles/s4159…
Colm Ryan @colmr
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Jun.-Prof. Kerstin Wi... @ECSignalMet
156 Followers 190 Following Since September 2021 the "Endothelial Signaling & Metabolism" Laboratory is part of the Institute for Cardiovascular Sciences at the University Hospital in BonnYou might like
