Background and Goals
In medicine, cooling induces metabolically suppressed state that preserves organs for transplantation and saves lives of trauma victims. In nature, it allows hibernating animals survive periods of inadequate food supply. To understand how cold induces cells to enter a protective dormant state, we use a simple animal model, the roundworm Caenorhabditis elegans, which was used to uncover many important biological processes form apoptosis to RNAi. When subjected to severe cold, C. elegans enter a hibernation-like state and some mechanism promoting cold survival in nematodes are conserved in mammals [1-3].
In this project, you will investigate specific transcription factors that we hypothesize function as “master regulators” of cellular hibernation. How do they “sense” the drop in temperature? Do they function in specific tissues? What pathways functioning downstream from these transcription factors that are necessary for cold survival and why? Do the identified factors/pathways also protect human cells from cold? Could their ectopic induction preserve cells in other physiological contexts, e.g. during aging? These are examples of the questions that can be addressed in this project.
Methods
The student will learn fundamentals of C. elegans and bacterial culture, molecular genetics, light and fluorescence microscopy, microinjection, and genome engeneering.
Contact Person
Dr. Pooja Kumari; pooja.kumari@ibv.uio.no
References
1. Pekec, T., et al., Ferritin-mediated iron detoxification promotes hypothermia survival in Caenorhabditis elegans and murine neurons. Nat Commun, 2022. 13(1): p. 4883.
2. Engelfriet, M.L., et al., Reprograming gene expression in 'hibernating' C. elegans involves the IRE-1/XBP-1 pathway. Elife, 2025. 13.
3. Habacher, C., et al., Ribonuclease-Mediated Control of Body Fat. Dev Cell, 2016. 39(3): p. 359-369.