@nstroustrup.bsky.social
A British/American group leader at @crg.eu . We study the biology of aging using molecular genetics, engineering, systems biology, and probabilistic machine learning. Lab page: http://lifespanmachine.crg.eu
Second this!
And of course, I remember his kindness of taking me on as a clueless engineering student and getting me a start in genetics. I only worked with him for a year, more than twenty years ago, but I still think about things he said.
David Botstein, 1942 - 2026.
www.online-tribute.com/DavidBotstein
So while David is often remembered for his field-defining technological advances, e.g. restriction fragment linkage mapping and microarrays, what I remember most is the way he spoke and thought--integrating complex mechanistic detail with broader ideas about yeast physiology and metabolism.
David was super smart and super direct, with a insistence on clear thinking that permeated everything he did. He could speak about "big picture" dynamical properties of cells, but he also had an encyclopedic memory-- ask him about any yeast gene and he'd tell you about it in fascinating detail.
hoping to learn what all the excitement was about, at the new genomics institute they'd just built on campus. I cold-emailed David looking for work, and a week later I was sitting in his office, learning about the principles of chemostats. I think I still have the little notebook drawing he made.
It's very sad to learn of David Botstein's passing. I worked in David's lab as an undergraduate--one of the most formative periods of my academic life and probably the biggest reason I work in biology today.
I vividly remember my first meeting with David. I was a 3rd year engineering student,
Very cool!
We found 24 neuron classes that are excited or inhibited by environmental H2O2, spread across the nose, mouth, and inner pharynx. Different neurons trigger at different H2O2 levels (from 1 µM early warning to >1 mM lethal), and many adapt, so responses encode dose + recent history. 7/
I am curious what counterfactual unsettling egg shapes you have in mind!
I was today years old when I discovered that "npj Aging" and "Nature Aging" are separate journals, despite being published with identical titles by Springer Nature!
Please consider joining us--the new restrictions on academic freedom are coupled with a move to make all syllabi public and secretly record our classes--UNC's status as a top public university is at stake
I knew about the downward part, but not the upward part, and now I'm not okay.
Happy International Day of Women and Girls in Science! 🧪 Don't forget to send in your nominations for the FEBS | EMBO #WomenInScience Award.
Deadline: 15 May
Read more:
https://www.embo.org/the-embo-communities/febsembo-women-in-science-awardees/nominate-for-the-women-in-science-award/
#award
sunday afternoon family collaboration
📣 Please spread: we’re hiring a Lab Manager! It is a critical position in our new lab. As our lab moves to Barcelona and joins the @crg.eu, we’re looking for a Lab Manager to help build the lab and set the lab atmosphere.
🔗 Apply here 👉 recruitment.crg.eu/content/jobs...
Surely people training on Wikipedia would just download the corpus, which is trivial to do, and analyze their local copy, which is orders of magnitude faster than crawling the website?
This was a lovely first read of 2026
"Results from experiments with N = 4 or less are shown to be highly misleading (...). For a cut-off of 2-fold expression differences, we find an N of 6-7 mice is required to consistently decrease the false positive rate to below 50%, and the detection sensitivity to above 50%"
Yet one more reason we cannot allow LLMs to serve as epistemic grounding is that we cannot triangulate among them the way you can among reasonable independent sources. They bullshit in the same way and end up agreeing with one other about things that are completely false.
Organelles do NOT have a single uniform pH.
And if you think they must, because “protons diffuse fast,” this paper is for you.
A thread on why that assumption is wrong; and what we found instead. 🧵 1/n
The manuscript is out now--take a look! www.nature.com/articles/s41...
We’d love feedback! As always, please reach out if you’re interested in getting more info or reagents. 10/10
We have transcriptomics data describing the on- and off-target effects of different AID system implementations. We also generated several new TIR1 lines we think will be useful to others, including a new “whole-body” line with pan-somatic and pan-germline expression. 9/10
One of the most exciting outcomes was that we figured out how to control two different proteins independently in the same living animal, a “dual channel” AID system that opens the door to cool new experimental designs. 8/10
Along the way, we ran into several surprises including some unexpected (and in some cases unfortunate) features of the popular AID2 system...it's worth taking a look at, for anyone using the AID2 system. 7/10
So we took a close look at existing AID implementations for use in quantitative degradation experiments. We ran careful dose–response experiments, and found it is possible to control the rate of an animal’s aging by quantitatively degrading components of IGF signaling. 6/10
Most people use AID in a binary way: adding lots of auxin to drive protein levels as low as possible. However, biology—especially aging and physiology—is rarely just “on” or “off.” What my group really wanted was a way to tune protein levels in a controlled, quantitative way.5/10
In 2009, the yeast biologists Kanemaki et al realized that they could take TIR1 out of plants and put it into other organisms--degrading any protein modified to include an AID tag. In 2014, Abby @adernburg.bsky.social, Jordan @gotworms.bsky.social, and others adapted it for C. elegans 🐛. 4/10
Our approach builds on the Auxin-Inducible Degron (AID) system, a technology derived from plant biology, where a protein called TIR1 triggers the degradation of any protein containing a short target peptide sequence—but only when activated by a specific hormone called Auxin. 3/10
Our lab studies the molecular genetics of aging--we want to understand why organisms grow old and how to engineer them to age better. 🛠️🧬💀That said, the technology I’m describing here should be useful well beyond aging, for anyone doing quantitative biology in eukaryotes. 2/10
