Memories can survive even after the brain temporarily loses more than half of its synaptic connections, according to a new mouse study in Science, which challenges the long-held view that long-term memories depend on stable individual synapses.
Learn more: https://t.co/6PbiaMd1F8
Dimensionality reduction can see structures that do not exist and miss structures that exist.
𝐓𝐡𝐞 𝐬𝐢𝐦𝐩𝐥𝐞𝐬𝐭 𝐞𝐱𝐩𝐥𝐚𝐧𝐚𝐭𝐢𝐨𝐧 𝐢𝐬𝐧’𝐭 𝐚𝐥𝐰𝐚𝐲𝐬 𝐭𝐡𝐞 𝐛𝐞𝐬𝐭 𝐨𝐧𝐞.
Sometimes, no simple way of describing the complexity of the data exists, at least not one that humans can readily interpret.
Then, faithfully representing the data is at odds with finding simple explanations.
“Everything should be made as simple as possible, but no simpler”
A basic intro video with some strategies how to avoid mistakes when using dimensionality reduction:
https://t.co/sND205WZue
What if you could watch chromatin states change inside living neurons.....IN REAL TIME? Repost or share if you or someone you know dreams of this!
The Solecki Lab is building an imaging-based biosensor platform to make chromatin biology visible, measurable, and experimentally testable as neurons mature and wire into brain circuits (see enhancer nucleosomes fluttering below).
We’re looking for an Associate Scientist who wants to do more than run experiments. Someone who wants to help build the framework for seeing how the neuronal genome changes as the brain is built.
This new #review from Sarah Hachmer and Dr. Jeffrey Dilworth (@EpigeneticsYOW) explores how transcriptional #enhancers help muscle stem cells interpret environmental signals during regeneration.
🔬 Learn more: https://t.co/GUTOnHTuvA
Indeed a great loss to the field. Had some brief discussions with him during my grad school. He was a womderful person. I havealways followed his work. RIP
A huge loss to the RNA biology field, but Greg’s legacy will continue to inspire and impact generations to come. 💕
Gregory J. Hannon (1964–2026): Cell https://t.co/BiOFGA7MKN
Our latest paper: RA signaling is known for its role in posteriorizing the body axis via Hox genes, we show that it is also crucial for the formation of the most anterior population of neural crest through Alx genes in the Hox-negative head region. https://t.co/qDvbS3Tqz0
Exciting breakthrough technology from the lab, now live in @CellCellPress ! Instead of cutting the genome where proteins bind (e.g., Cut&Tag), D&D-seq scars the DNA with a deaminase, allowing single cell genome mapping of TFs and chromatin remodellers!
New preprint alert! 🚀 Across 60 human cancer cell lines spanning 20 cancer types, single-cell RNA+ATAC reveals pan-cancer cell-state heterogeneity, core gene-regulatory networks, and an EMT axis conserved across tissue origins.
Huge congrats to first author @xu_zxu, who recently defended his PhD, and Aileen Ugurbil from our lab @RockefellerUniv! https://t.co/4fNQJlJY3m
🌟G&D SPOTLIGHT 🌟
G&D is pleased to present a collection of recent articles on RNA biogenesis and regulation.
Learn more about small RNA biogenesis, target-mediated miRNA degradation, RNA splicing, ribonucleoprotein granules, and more.
➡️ https://t.co/3WkTKWhUfI
Large-scale transcriptomic data across four mammalian species and multiple tissues identify conserved molecular signatures associated with ageing and mortality risk.
The integration across species, tissues, perturbations, and interventions is a notable strength. Further, mRNA abundance is more biologically interpretable than DNA methylation, though still an indirect readout of physiological processes.
The article advances the idea that ageing is multidimensional rather than a single scalar process, with partially separable inflammatory, metabolic, extracellular matrix, and stress-response programs changing over time.
Predictive performance is strong, but it is important to distinguish predictive association from mechanistic understanding. Even sophisticated transcriptomic signatures primarily capture statistical dependencies and correlations with ageing-related states and mortality risk. They do not yet explain the causal mechanisms underlying ageing.
Achieving deeper mechanistic understanding will require more functional readouts: protein states and modifications, molecular interactions, metabolic fluxes, cell functions, tissue physiology, and experimentally testable causal perturbations.
This work provides a valuable cross-species resource and advances the field through its scale, comparative framework, and integrative systems biology perspective.
Today we all lost our jobs.....
Three Nature papers showing that scientists in the conventional sense are obsolete
At least read the first one.... the AI replaced all things that the scientist does ....
https://t.co/zMsRLaaRDU
Our paper in @Nature today 🥳 We tracked 6,438 mice from puberty to death and mapped the genetics of *when* you die, not just whether a gene associates with lifespan.
https://t.co/EoeexqJoHk
59 loci. Two decades of data. Thread 👇
#Longevity#Aging#Genetics#Healthspan
Big news: Our Virtual Embryo project has been selected as a Laude Institute Moonshots Seed Grant winner — chosen from 125 proposals evaluated by 600+ leading researchers.
I’m deeply honored to be recognized alongside a remarkable community that includes Fields Medalists like Terence Tao, Nobel laureates like Michael Kremer, Turing Award winners like Raj Reddy, and creators of transformative tools such as Jupyter Notebook.
We are now building (1) the largest time-resolved organism-level 3D perturbation atlas of mouse embryogenesis; (2) what could become the first digital twin of mammalian embryogenesis — a predictive model of development designed to uncover the mechanisms of congenital disease and ultimately help ensure that every newborn has the healthiest possible start in life.
If this vision excites you, come build with us — alongside Emily Fox, James Zou (@james_y_zou), and Marinka Zitnik (@marinkazitnik).
Thank you to @LaudeInstitute for believing in this vision. We also welcome industrial and philanthropic partners who want to help shape the future of developmental biology and human health.
PerturbFate is officially out in @Nature today! From chromatin to RNA, we dissect the causal regulatory logic linking genotype to phenotype. Huge thanks to my PhD advisor @junyue_cao@Wei_Zhou_1989, and @RockefellerUniv for providing such an incredible research home!
Years in the making: a detailed aging gene signature in mice and rats. >30 tissues, high Ns, multi-time points throughout the lifespan. >5000 samples in total. The data is accessible, so you check to see if your favorite gene is age-regulated.
https://t.co/5heN6ixvt1