Today we said farewell to our PhD student turned postdoc Eugene Ballhysa. The energy in his conversations matched his enthusiasm for science🔬🐟We’ll miss you—and we wish you all the best for the road ahead!
🥳🎓Congratulations to Maja on an outstanding master’s thesis defense. Your rigor, perseverance, and dedication are exemplary. Excited to see what comes next.🌟 #GradLife #MastersDefense
4/4 Perturbing either the mitochondrial ribosome or the RNase P/MRP complex restores ribosomal balance & extends lifespan, suggesting that improving ribosome coordination, rather than reducing overall biogenesis, is a promising avenue to support cellular health in ageing.
3/4 Using C. elegans, we find that loss of the nucleolar regulator, ncl-1/TRIM2-3, disrupts ribosomal balance, leading to proteostasis defects and premature aging. Ribosomal biogenesis becomes uncoordinated, causing imbalanced ribosomal components and translational dysfunction.
2/4 In this study, we investigate fundamental questions about ribosome biology and ageing. While ribosomes are essential to life, how their assembly and coordination change with age, and how that contributes to ageing, remains poorly understood.
1/4 Our preprint “Modulation of the RNase P/MRP complex and mitochondrial ribosome enhances cytosolic ribosome coordination and sustains longevity” is now live @biorxivpreprint.bsky.social 📄 #agingbiology #ribosome 👉www.biorxiv.org/content/10.64898/2026.02...
Our tiny market of longevity dreams—lab merch, publications, Flammkillifish and ‘rejuvenation’ tonics—won🥈in the annual window decoration contest!🥇to the @inahuppertz.bsky.social and Scheiblich labs chasing the Grinch for their data. Backups, people! 💾 #LabLife #AgingResearch #FestiveScience
From worms to humans, our lab gathered for the annual festive brunch and Secret Santa—because community is the best longevity intervention🎁🎄🫶 #LabLife #Longevity #ScienceCommunity
🚨New @biorxivpreprint: We model the splicing factor disease Verheij syndrome using C. elegans. Disruption of methionine and phospholipid metabolism drives growth defects; vitamin #B12 restores metabolic balance and rescues development! #metabolism #Celegans #RNAsplicing
doi.org/10.1101/2025...
Eugene, Victoria & Tabrez are just back from Copenhagen🇩🇰 #ARDD2025! Kazuto (@kkawamura13.bsky.social) took the stage to share his insights on fasting-refeeding and age-restoration. ⌛️🍽️ Turns out, the fountain of youth might just be a histone away!🪱🔬 #Rejuvenation #AgingResearch
Our lab's BBQ last Friday was a blast! Meticulous research revealed the ultimate anti-aging formula: juicy burgers and great company! 🍔👩🔬 #AgingResearch
🏆⚽️ A huge shoutout to the Antebi lab's team 'C(riminally) elegant' for winning the human Foosball match at the CECAD Summer Party @cecad.bsky.social! Your elegance on the field is unmatched!💪 #LabLegends #Foosball
7/7 In sum, hlh-30 mutation causes misalignment of nutrient cues and growth signaling, resulting in DNA damage & cellular senescence, which abrogates stem cell and organismal longevity. Cellular senescence is an evolutionarily ancient response to damage conserved even in C. elegans.
6/7 Together with Manuel Serrano’s group, we found that TFEB loss reduces survivorship in both embryonic and cancer diapause, and that TFEB and TGFβ signaling are regulated during diapause. Hence, targeting TFEB might undermine cancer dormancy and prevent relapse in vivo.
5/7 HLH-30 downregulates TGFβ signaling from neurons to germline stem cells, promoting stem cell quiescence upon ARD to safeguard against cellular senescence. Mutations in TGFβ signaling prevent senescence upon hlh-30/TFEB loss, restoring resilience and reproductive competence.
4/7 Genetic suppressor screens reveal mutations that disrupt TGFβ, cGMP and insulin/IGF signaling potently reverse hlh-30/TFEB collapse.
3/7 hlh-30/TFEB is a master regulator of ARD, whose loss leads to complete collapse during ARD and recovery. Mutants arrest in a novel senescent-like state never described before in worms, and germline stem cells show features strikingly similar to mammalian cellular senescence.
2/7 Worms fasted in late larval development progress to a sleep-like quiescent state called the adult reproductive diapause (ARD) and can survive for months without food. Upon refeeding they undergo restoration, regenerating germline, soma and reproduce.
1/7 🚨Out now @nataging.nature.com 🚨 We identified a genetic network of TFEB, TGFβ and NOTCH signaling regulating stem cell resilience, rejuvenation & senescence in C. elegans in response to nutrient cues, with conservation across taxa. www.nature.com/articles/s43...
3/7 hlh-30/TFEB is a master regulator of ARD, whose loss leads to complete collapse during ARD and recovery. Mutants arrest in a novel senescent-like state never described before in worms, and germline stem cells show features strikingly similar to mammalian cellular senescence.
2/7 Worms fasted in late larval development progress to a sleep-like quiescent state called the adult reproductive diapause (ARD) and can survive for months without food. Upon refeeding they undergo restoration, regenerating germline, soma and reproduce.
Photo shows the CGA PhD students of the graduating class of 2021.
🎊Today, we're excited to celebrate the graduation of our amazing 13 students from the CGA Class of 2021! We’re so proud of all their accomplishments.
🎓Come join us now as they present their PhD projects at the 13th CGA Graduate Symposium.
And, of course, we can’t wait for the dinner party tonight!🍾
🥳Congratulations @annadiederich01.bsky.social for successfully defending your master's thesis. Great collaboration with the Demetriades Lab. We are thrilled to also accompany you on your PhD journey. To many more interesting findings! 🥂
Tim receiving a farewell gift from Eugen. Both are standing in a meeting room, smiling and holding the gift between them.
Last week we said goodbye to our PhD student-turned-postdoc Tim! We are sad to see you go, but confident that you will do great things wherever your journey takes you next! 👨🔬#Farewell
👩🎓We're thrilled to share some wonderful news! Klara Schilling from the CGA Class of 2020 successfully defended her PhD thesis today!
Klara, we hope you're enjoying some well-deserved celebrations right now! 🥂🎊 @mpiage.bsky.social @antebilab.bsky.social
To sum up, hil-1/H1-0 is a critical mediator that reprograms epigenetic state in response to metabolic inputs. We believe studying refeeding after a prolonged fast can help elucidate adult organismal rejuvenation in a natural context.
Looking at the flip side of the coin, hil-1 is an equally important regulator of the refeeding response. Further enhancing the natural downregulation of hil-1 during refeeding by RNAi improved restoration, as measured by body size regrowth and functional muscle regrowth.
Loss of HIL-1/H1.0 reduced survival during prolonged fasting in C. elegans worms and in a human in-vitro model for nutrient restriction, suggesting that this epigenetic factor has a key role in promoting adaptation to quiescent and low nutrient states.
What regulates the fasting-refeeding switch? Unexpectedly, we found a linker histone regulated by nutrients and mTOR signaling, that promotes resilience during fasting and restoration upon refeeding. Its regulation is evolutionarily conserved, including in fasted human patients.
Rejuvenation of gene expression patterns also occurred in refed killifish, suggesting refeeding as a time window for age restoration from simple worms to vertebrates!
