Barbara Conradt
Associate Professor of Genetics
Research Areas: Developmental Biology, Genetics, Regulation of Gene Expression
Regulation and mechanisms of programmed cell death and mitochondrial dynamics
Programmed cell death is the physiological process through which multicellular organisms eliminate superfluous or potentially harmful cells from their body. Deregulated programmed cell death can lead to various types of diseases in humans, including cancer, autoimmune disorders and neurodegenerative diseases. Analyses on the regulation and mechanisms of programmed cell death will therefore not only help us understand the functions of this process in cellular homeostasis, but its roles in various pathological processes. To that end, we are studying apoptotic cell death during the development of the nematode Caenorhabditis elegans, which has proven to be particularly amenable to cell death studies. Specifically, using genetic and molecular approaches, we are analyzing the regulation and function of members of the BCL-2 family of proteins, which are crucial regulators of apoptotic cell death in animals as diverse as nematodes and mammals.
Mitochondria are highly dynamic organelles that constantly divide and fuse. The morphology of mitochondria in a particular cell or cellular context is determined by the relative rates of mitochondrial fusion and division and can range from a highly tubular network to individual, punctuate organelles. Very little is known to date about how the rates of mitochondrial fusion and division are regulated. In addition, it is still unclear what the consequences of changes in mitochondrial morphology are with respect to the function of a particular mitochondria, cell or organism. To address these questions, we are studying mitochondrial morphology changes in C. elegans. In particular, using genetic, molecular, and cell biological approaches, we are studying the regulation and functions of members of the family of dynamin-related GTPases, which have conserved roles in mitochondrial dynamics.
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Publications
Rolland, S., Lu, Y., David, C. N. and Conradt, B. (2009). The BCL-2-like protein CED-9 of C. elegans promotes FZO-1/Mfn1, 2- and EAT-3/Opa1-dependent mitochondrial fusion. J. Cell Biol. In press.
Conradt, B. Genetic control of programmed cell death during animal development. (2009). Annual Review of Genetics. In press.
Nehme, R. and Conradt, B. (2009). egl-1, a key activator of apoptosis during C. elegans development. Oncogene. In press.
Hatzold, J and Conradt, B. (2008) Control of apoptosis by asymmetric cell division. PLoS Biol. Apr 8;6(4):e84.
Schertel, C. and Conradt, B. (2007) C. elegans orthologues of components of the Rb tumor suppressor complex have distinct pro-apoptotic functions. Development 134:3691-3701.
Schertel, C. and Conradt, B. (2007) C. elegans orthologues of components of the Rb tumor suppressor complex have distinct pro-apoptotic functions. Development (in press).
Grote, P. and Conradt, B. (2006) The PLZF-like protein TRA-4 co-operates with the Gli-like transcription factor TRA-1 to promote female development in C. elegans. Dev Cell 11:561-573.
Jagasia, R., Grote, P., Westermann, B. and Conradt, B. (2005) DRP-1-mediated mitochondrial fragmentation during EGL-1-induced cell death in C. elegans. Nature 433:754-760.