Cells in a living organism need to be able to readily respond to changes in nutritional status. Upon starvation, certain tissues respond by autophagy, to provide energy and building blocks to sustain essential cellular functions.
Importantly, these cells must also turn off autophagy when nutrient supplies are replenished, because unrestricted autophagy is harmful to cellular fitness.
Surprisingly little is known about how autophagy is terminated, especially in the context of a multicellular organism. We work on uncovering and understanding novel mechanisms of autophagy termination, using Drosophila as a model.
... and how does this affect sleep?
See more about the Sleep and autophagy project
LC3 (green) and p62 (magenta) in patient-derived kidney organoid
Each year around 800 people are diagnosed with kidney cancer in Norway. Whereas localized cancer can be cured by surgery, the challenge is to identify which patients will progress to metastatic cancer and also to identify the best treatment for each of those patients.
We are working on the use of markers of autophagy to address these needs in different subtypes of renal cell carcinoma and also in the inherited predisposition for renal cancer associated with Birt-Hogg-Dubé syndrome.
Lymph gland with "leukemic" phenotype in Drosophila melanogaster
Chromosomal rearrangements of the MLL gene are associated with development of high-risk acute leukemia. MLL-rearranged (MLL-r) leukemia is treated with aggressive chemotherapy, but patients often relapse and survival rates are dismal. Clearly, there exists a need for novel forms of therapy.
However, development of new treatment is hampered by our very limited understanding of the genetic framework that underpins MLL-r leukemia.
We are working on unraveling this genetic framework, by taking advantage of the of the powerful genetic tools of Drosophila in a fly model of MLL-r leukemia, where we perform genetic modifier screens and study effects on the hematopoietic system of Drosophila larvae.