Cells adjust their proteome to environmental conditions, but it remains unclear whether the proteome can be transmitted from parents to offspring. This study analyses the intergenerational effects of dietary restriction in C. elegans and shows that maternal mTORC1 activity governs the transfer of ribosomes, thereby modulating early growth and development.

Animals must continually adjust their proteome to match environmental conditions, but it is unclear whether the proteome can be propagated from parent to offspring. This Primer explores a recent study...

Cells adjust their proteome to environmental conditions, but it remains unclear whether the proteome can be transmitted from parents to offspring. This study analyses the intergenerational effects of dietary restriction in C. elegans and shows that maternal mTORC1 activity governs the transfer of ribosomes, thereby modulating early growth and development.

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

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

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.

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

Friedrich Miescher Institute, open position

Agroscope sucht Wissenschaftliche/-r Mitarbeiter/-in Bodenmonitoring

Professor Alexei Maklakov, Biological Sciences, University of East Anglia – contact me Professor Tracey Chapman, UEA BIO Professor Simone Immler, UEA BIO Why do organisms age?

PhD Project - PhD in Quantitative Biology of Development and Aging at University of Bern, listed on FindAPhD.com

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