The public defence will be held as a video conference over Zoom.
The digital defence will follow regular procedure as far as possible, hence it will be open to the public and the audience can ask ex auditorio questions when invited to do so.
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Digital trial lecture - chosen topic - time and place
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Digital trial lecture - given topic - time and place
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Adjudication committee
- First opponent: Professor Emanuel Rosonina, York University, Toronto, Canada
- Second opponent: Professor Ian Willis, Albert Einstein College of Medicine, New York, USA
- Third member and chair of the evaluation committee: Associate Professor Valeria Vitelli, Institute of Basic Medical Sciences, University of Oslo
Chair of defence
Associate Professor Ragnhild Eskeland, Institute of Basic Medical Sciences, University of Oslo
Summary
Cells must constantly adapt to life threatening changes of their environment. Each of these stresses triggers a specific cellular response. For instance, drops in nutrient availability are sensed by the so-called Target-Of-Rapamycin Complex 1 (TORC1). TORC1 regulates the switch from promoting cell growth under nutrient rich conditions to catabolic survival under nutrient depletion. In addition, posttranslational modification of protein by the Small Ubiquitin-like Modifier SUMO has been shown to participate in the cellular response to stress via the Sumo stress response (SSR).
Using Saccharomyces cerevisiae and high throughput methods, we revealed mechanisms by which Sumoylation and TORC1 support survival upon nutrient stress. Both pathways regulate the transcription of genes involved in the costly process of translation: ribosomal protein genes and tDNA.
We further showed that Sumo regulation of tDNA transcription occurs not only in response to nutrient stress but also in response to other cellular injuries (i.e. heat, oxidative and osmotic stress, and DNA damages).
Using metabolomics approaches, we then found that hyposumoylation depletes certain families of amino acids and key intermediary metabolites of glycolysis and synthesis of nucleotides. These findings suggest that sumoylation also participates in anabolic processes through other pathways than transcription.
Finally, we addressed another aspect of nutrient stress response: autophagy. Using a fluorescence microscopy-based genetic screen we discovered genes that were previously not associated with the autophagic process. Some of these genes are involved in the activation of autophagy upon starvation and others in its inhibition upon refeeding.
In this work, we improved the understanding of several aspects of cellular response to different stresses with a particular focus on nutrient stress response. Furthermore, we shed light on the role of the sumoylation pathway in physiological and perturbed growth conditions.
Additional information
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