We need to understand how #Covid_19 affects the brain. Our study out now at @Nature provides a molecular basis. Terrific experience, sharing co-first with @andcyang and exceptional guidance by Tony @wysscoray and Andreas Keller. Free link: @Stanford_Neuro

RT @fbaumdicker: If you are interested in microbial #pangenomes, join us @eseb2025 in Barcelona with Jesse Shapiro and Anna Dewar. Only two….

RT @AdlungLab: One thing we know, another thing we can't avoid: Infection and aging partially converge in spatial transcriptomics data of m….

New preprint alert 🥁📣 We present 168 #spatial #transcriptomics samples (Visium + Stereoseq) - Annotating 100 molecular niches across mouse organs and finding spatial DEGs / pathways shared between #aging and systemic #infection. Pls share and read more

RT @ZucheroLab: Congrats to the team again, and thanks to Dr. Andrew Olson for imaging this beautiful #oligodendrocyte #cytoskeleton featur….

Thanks to all our collaborators, especially for @iram_tal and @ZucheroLab for making this a success story and a great experience🚀! In science, tenacity always pays off 🎉🥳.

Paper accepted in @PNASNews ! Stay tuned. 📈🥳.

Tired of trying to grab your favorite 🧠-gene from countless papers? Search no more!.Our new region-aware atlas #zebra, based on a deep neural network gives you easy access to over 4 million sc/snRNA-seq profiles across the🧓&🐭brain in age and disease:

RT @Oliver__Hahn: Thrilled to see our map of the aging mouse brain published in @CellCellPress. We find that white matter tracts are hotsp….

RT @Helmholtz_HIPS: Great opportunity in the lab of Alex Titz and many more at HIPS and @Saar_Uni. We have a total of 15 open PhD positions….

Glad to share our paper mapping small noncoding RNA across the mouse lifespan and in 16 organs @CCB_CBI Map was augmented by rejuvenation intervention and vesicle sequencing. Strongest reversable effects occurred in the aging liver, mediated by miRNAs:.

RT @NatureBiotech: Characterizing expression changes in noncoding RNAs during aging and heterochronic parabiosis across mouse tissues https….

RT @benbfly: An incredible and badly needed resource for disease epigenetics. Complete methylomes for individual cell types purified from n….

The future of spatial is here! Big shout out from the @10xGenomics Symposium in freezing and beautiful Munich🏔. A great get-together of young (and old) #Spatialists and now, new friends from @HelmholtzMunich! Proud to see the community making incredible progress #Visium #Xenium

There’s much to explore in the supplement, give it a try. We are also happy to receive your questions or comments. Thank you for staying with me until this point and again a big shout out to all team members for their great work! 🙏.

In summary, we could show how the SRF pathway essentially enables mammalian #myelination by powering up the actin cytoskeleton machinery needed for OLs to get in move rather than promoting the actual differentiation process. They are the #strangers wrapping our neurons.

Now knowing that SRF drives early actin assembly we quantified the amount of filament levels from purified OPC over the differentiation axis, comparing wildtype against knockout. We confirmed that the actual assembly but not the disassembly process was disrupted in the latter.

Tracking binding sites of the CArG consensus motifs, we found OPC/OL shared target gene sets from the actin machinery. Exactly those genes were primarily down-regulated in our knockout experiment – we uncovered a positive regulation of actin cytoskeleton by SRF in the OL lineage!

Hypothesizing that SRF regulates key players of the actin cytoskeleton assembly, which is needed for the morphological transformation, i.e. getting in contact with axons, we performed cell-type specific #ChIPseq to determine its targets.

After confirming that the density of OPCs and OLs was not affected by our knockout, we wanted to have a mechanistic understanding on how SRF modulates the cells’ ability get in contact with axons using #RNAseq. We found an enrichment for cytoskeletal genes being dysregulated.

Generating a mouse model carrying a targeted SRF knockout in OPCs we found a surprising phenomenon: Missing the transcription factor causes a significantly lower number of myelinated axons, while those which still got myelinated showed the same thickness than the wildtype.