Antebi Lab

🏆⚽️ 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.

A TFEB–TGFβ axis systemically regulates diapause, stem cell resilience and protects against a senescence-like state - Nature Aging Nonninger et al. identify the TFEB–TGFβ signaling axis as a regulator of stem cell resilience that protects against a senescence-like state during the adult diapause in Caenorhabditis elegans, a mecha...

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!

Can organisms reverse their biological age? In the worm C. elegans we found striking biological age restoration during refeeding after a prolonged fast, based on aging clocks! Fasting is usually linked to anti-aging, but our study points to the age-restorative role of refeeding.

Resilience and restoration from fasting-refeeding mediated by a nutrient-regulated linker histone Intermittent fasting and fasting-refeeding regimens can slow biological aging across taxa[1][1]. Shifts between fed and fasted states activate ancient nutrient-sensing pathways which alter cellular an...

Preprint alert @biorxivpreprint! We are excited to share our latest study led by @kkawamura13.bsky.social @annadiederich01.bsky.social in collaboration with & C. Demetriades Lab & @muellerrom.bsky.social Lab
www.biorxiv.org/content/10.1...