Benjamin Towbin

Tenure-track Assistant Professorship in #Quantitative #Cell #Biology at the ICB @unibern. Apply until 17 October. Combination of theory/computation and experiments particularly encouraged. Please repost!

www.nature.com/naturecareer...

Assistant Professor with tenure-track for Quantitative Cell Biology (80-100%) - Bern, Switzerland job with University of Bern, Institute of Cell Biology | 12840798 Assistant Professor with tenure-track for Quantitative Cell Biology (80-100%) at the University of Bern, Switzerland.

Exciting opportunity for TT-Ass #Professorship in Quantitative Cell Biology
@unibe.ch @izb-unibern.bsky.social! Applicants combining experimental and computational approaches/theory are particularly encouraged. Great colleagues, environment, infrastructure. What's not to like?
tinyurl.com/42f3p863

What is this?

Last chance to submit an abstract for the LS2 Systems Biology Symposium! Extended deadline: Sunday, 27.4.

✅Present your work in interactive talk sessions!
✅Get feedback from your peers!
✅Find the collaborator that solves all your problems!

Submit now & rest on the weekend!

Warm memories of a defining time...
So sad to have missed this.

אין כמו אורי!

Last chance to submit an abstract for the LS2 Systems Biology Symposium! Extended deadline: Sunday, 27.4.

✅Present your work in interactive talk sessions!
✅Get feedback from your peers!
✅Find the collaborator that solves all your problems!

Submit now & rest on the weekend!

Compression of morbidity by interventions that steepen the survival curve - Nature Communications Longevity research aims to extend lifespan and reduce sickspan in aging. Here, the authors show that only interventions that steepen survival curves can compress the sickspan relative to lifespan.

Our latest on aging, where we reveal an unexpected link between healthspan and equality of lifespans.
By @y1fanyang.bsky.social , out now @naturecomms.bsky.social
www.nature.com/articles/s41...

Every Progress Report

📢Join us tomorrow, Friday, March 28th at 10:00, for an exciting talk by @olmedo-lab.bsky.social at the ICB!

She’ll be presenting:
"Maintenance of cell quiescence during starvation in C. elegans"

Don’t miss this opportunity to dive into fascinating research! More info on our website: izb.unibe.ch

Congratulations to Jana Brunner on successfully defending her PhD this week! 🎉 Jana investigated the molecular mechanisms of developmental timing in the worm C. elegans 🪱

early career researchers: Do not miss this oportunity to present and discuss your work with an expert audience!

🚨 Join us for the LS2 Swiss #Systems #Biology Symposium in Bern!

❌ to talk marathons
✔️ to new connections and interactions

➡️Mini parallel sessions with Q&A during the talks.

Keynotes by @ehannezo.bsky.social @leeat-keren.bsky.social

tinyurl.com/5hf485ee

@lifesciswitzerland.bsky.social

Eukaryotic Elongation Factor 2 Kinase EFK-1/eEF2K promotes starvation resistance by preventing oxidative damage in C. elegans | Nature Communications Cells and organisms frequently experience starvation. To survive, they mount an evolutionarily conserved stress response. A vital component in the mammalian starvation response is eukaryotic elongation factor 2 (eEF2) kinase (eEF2K), which suppresses translation in starvation by phosphorylating and inactivating the translation elongation driver eEF2. C. elegans EFK-1/eEF2K phosphorylates EEF-2/eEF2 on a conserved residue and is required for starvation survival, but how it promotes survival remains unclear. Surprisingly, we found that eEF2 phosphorylation is unchanged in starved C. elegans and EFK-1’s kinase activity is dispensable for starvation survival, suggesting that efk-1 promotes survival via a noncanonical pathway. We show that efk-1 upregulates transcription of DNA repair pathways, nucleotide excision repair (NER) and base excision repair (BER), to promote starvation survival. Furthermore, efk-1 suppresses oxygen consumption and ROS production in starvation to prevent oxidative

EFK-1/eEF2K in C. elegans enhances starvation resistance by preventing oxidative damage. Crucial for survival & linked to eEF2 phosphorylation. #BioResearch PMID:39966347, Nat Commun 2025, @NatureComms https://doi.org/10.1038/s41467-025-56766-1 #Medsky #Pharmsky #RNA 🧪

Are you thinking about yourself or the students? 😀. After 2hrs of teaching, i feel typically like i ran a cognitive marathon...

Job opening in my research group!! Please share.

I'm looking for a lab technician to join my small team investigating how chromatin structure regulates gene expression in C. elegans.

www.fmi.ch/education-ca...

Amazing stuff!

Thanks!

Thanks!

Thanks!

Thanks. Still thinking about an appropriate walk up song for this 🙃.

Thanks! We do not exclude an additional role for modifications/heterogeneity. But our data suggests that levels are at least sufficient for the effects observed: direct (and presumably modification unspecific) depletion of R-proteins to a similar degree had the same effect on growth as maternal DR.

Very interesting!
I wonder if ribosome heterogeneity us also seen here (i.e. some but not all ribosome variants are affected) or a really global effect.

cc @odedrechavi.bsky.social

Check out the new preprint from the Towbin Lab!

Intergenerational control of ribosomes under dietary restriction

Read full article here: biorxiv.org/content/10.1...
Thanks to our collaborator
@nstroustrup.bsky.social, @snsf-ch.bsky.social
for funding, and
@embl.org / @embo.org YIP for proteomics support.

In summary, we find that intergenerational control of core cellular machinery, such as the ribosome, can transmit information about the metabolic state from parent to offspring. This intergenerational control may prime offspring for their expected environmental conditions.

The control of progeny ribosomes involved specific regulation in the mother: soma-specific maternal inhibition of mTOR signaling fully recapitulated the effects of maternal dietary restriction, suggesting that mTOR transmits information across the germline-soma boundary.

Reduced ribosomes had physiological consequences: when offspring were switched to abundant food, they grew slower until they had restored normal ribosome levels. Thus, their translation capacity became a developmental bottleneck.

We explored this question using #dietary #restriction of #Celegans combining #proteomics and live #imaging. We found that while most proteins are reset between generations, ribosomal proteins remained low also in the offspring of dietarily restricted mothers.

Unlike microbes, animals face a unique challenge: Bacteria inherit their ribosomes passively through cell division. But in animals, soma and germline are physcially separated - So, is the proteome reset at every generation, or can parents influence the proteome of their kids?

In bacteria, studies going back to 1950s showed that the growth rate and ribosome expression are indeed tightly connected by a linear relation called the “growth law”. But such growth laws have rarely been studied in animals.