Expression of activated alleles of ras and JNKK
(rasVal12 and Hepact) causes the appearance of
malignant, invasive tumors in the Drosophila brain
(lower panel). Differentiated Neurons are labeled in
red, Tumor cells in green, and the actin
cytoskeleton in blue
The Bohmann lab uses Drosophila genetics, tissue culture approaches and biochemistry to model aging, cancer and metabolic regulation. Genetic, genomic, molecular and cell biological techniques are combined to achieve a systems level understanding of these complex processes.
Specific current projects include studies on JNK, Fos, Foxo and Nrf2 dependent signaling and gene regulation in oxidative stress response and aging. We are also working on signaling pathways that control malignancy in an in vivo cancer model. A recent focus of interest concerns the role of matrix metallo proteases in developmentally controlled as well as pathological cell movements and tissue invasiveness.
Current Research Projects
Barone MC, Sykiotis GP, Bohmann D (2011). Genetic activation of Nrf2 signaling is sufficient to ameliorate neurodegenerative phenotypes in a Drosophila Parkinson's model. Disease Models and Mechanisms, 4, 701-707.
Sykiotis GP, Bohmann D (2008). Keap1/Nrf2 signaling regulates oxidative stress tolerance and lifespan in Drosophila. Developmental Cell, 14, 76-85.
Wang Q, Uhlirova M, Bohmann D (2010). Spatial Restriction of FGF Signaling by a Matrix Metalloprotease Controls Branching Morphogenesis. Developmental Cell 18, 157–164.
Sykiotis GP, Bohmann D (2010). Stress-Activated Cap'n'collar Transcription Factors in Aging and Human Disease. Sci. Signal. 3, re3.