|
Return to: College of Biological Sciences: Medical School: U of M Home |
|
|
|
|
||
 |
|||||||
 |
|||||||
 |
|||||||
|
|
||||||
 |
|||||||
|
|
||||||
 |
|||||||
|
Areas of Research Strength: Developmental Mechanisms Genetic Mechanisms Cell Interactions Signal Transduction Cell Cycle Regulation back to top |
||||||
|
|||||||
|
Research Techniques: back to top |
||||||
|
|||||||
|
Research Interests: The Neufeld lab is interested in the basic mechanisms of cell growth control. They use the fruit fly Drosophila as a model system to investigate signaling pathways and cellular functions that regulate growth. The goal of their research is to understand how signals that control cell growth, such as nutrient conditions and growth factors, are connected to growth-promoting cellular processes such as nutrient uptake and biosynthesis. They focus on the target of rapamycin (TOR) protein kinases, which are central regulators of cell growth whose function is conserved from yeast to plants to mammals. TOR activity is controlled by nutrient levels, cellular energy state, and growth factors such as insulin, and in turn TOR controls multiple cellular functions critical for growth. Inappropriate activation of TOR signaling underlies a number of growth-related genetic diseases including cancer. In the lab, the approach is to identify mutations in genes involved in TOR signaling, and to characterize their function using multiple cellular and genetic assays. A second, related area of the lab's research centers on the degradative process known as autophagy. This process, which is controlled by the TOR pathway and induced by starvation, involves the non-selective engulfment and degradation of cytoplasm within the lysosome. Through autophagy, macromolecules and entire organelles are recycled into amino acids, lipids, and other simple molecules, thus supplying the cell with an internal source of nutrients under starvation conditions. Although autophagy has been understood morphologically for many years, the past decade has seen a new surge of interest in autophagy due to the recent discovery of approximately 20 “ATG” genes that regulate autophagy, and to the discovery that defects in autophagy are involved in aging, neurodegeneration, and cancer. The lab hopes to use the genetic tools available in Drosophila to define the functions and regulation of autophagy. back to top |
||||||
|
|||||||
|
Selected Publications: Knox, S., Ge, H., Ren, Y., Dimitroff, B. D., Howe, K. A., Arsham, A. M., Easterday, M. C., Neufeld, T. P., O’Connor, M. B. & Selleck, S. B. 2007. Mechanisms of TSC-mediated control of synapse assembly and axon guidance. PLoS ONE, in press. Juhasz, G., Puskas, L. G., Komonyi, O., Erdi, B., Maroy, P., Neufeld, T. P., & Sass, M. 2007. Gene expression profiling identifies FKBP39 as an inhibitor of autophagy in Drosophila. Cell Death and Differentiation, in press Hennig, K. M., Colombani, J., & Neufeld, T. P. 2006. TOR coordinates bulk and targeted endocytosis in the Drosophila melanogaster fat body to regulate cell growth. Journal of Cell Biology 173(6): 963-974. Scott, R. C., Juhasz, G., & Neufeld, T. P. 2007. Direct induction of autophagy by Atg1 inhibits cell growth and induces apoptotic cell death. Current Biology, 17(1):1-11. Hennig, K. M., Leopold, P., & Neufeld, T. P. 2006. Target of Rapamycin regulates bulk and targeted endocytosis to promote cell growth. Journal of Cell Biology, in press. Juhasz, G. & Neufeld, T. P. 2006. Autophagy: a forty year search for a missing membrane source. PLoS Biology 4(2):e36 Zhang, Y., Billington, C. J., Pan, D., & Neufeld, T. P. 2006. Drosophila Target of Rapamycin kinase functions as a multimer. Genetics 172(1):355-62. Cygnar, K. D., Gao, X., Pan, D., Neufeld, T. P. 2005. The phosphatase subunit Tap42 functions independently of TOR to regulate cell division and survival in Drosophila. Genetics 170:733-40. Scott, R.C., Schuldiner, O., Neufeld, T.P. 2004. Role and regulation of starvation-induced autophagy in the Drosophila fat body. Developmental Cell 7:167-178. Neufeld, T.P. 2003. Body building: regulation of shape and size by PI3K/TOR signaling during development. Mechanisms of Development 120:1283-1296. Hennig, K. M. & Neufeld, T. P. 2002. Inhibition of cellular growth and proliferation by dTOR overexpression in Drosophila. genesis 34:107-110. Zhang, H., Stallock, J. P., Ng, J. C., Reinhard, C., & Neufeld, T. P. 2000. Regulation of cellular growth by the Drosophila target of rapamycin, dTOR. Genes & Development 14:2712–2724. Gao, X., Neufeld, T. P., & Pan, D. 2000. Drosophila PTEN regulates cell growth and proliferation through PI3K-dependent and -independent pathways. Developmental Biology 221:404-18. Weinkove, D., Neufeld, T. P., Twardzik, T., Waterfield, M. D., & Leevers, S. J. 1999. The Drosophila class IA PI3K and its adaptor are autonomously required for imaginal discs to achieve their normal cell size, cell number and organ size. Current Biology 9:1019-1029. Neufeld, T. P., de la Cruz, A. F. A., Johnston, L. A., & Edgar, B. A. 1998. Coordination of growth and cell division in the Drosophila wing. Cell 93: 1183-1193. Neufeld, T. P., Tang, A. H., & Rubin, G. M. 1998. A genetic screen to identify components of the sina signaling pathway in Drosophila eye development. Genetics 148: 277-286. Neufeld, T. P. & Rubin, G. M. 1994. The Drosophila peanut gene is required for cytokinesis and encodes a protein similar to yeast putative bud neck filament proteins. Cell 77: 371-379. To view these and other publications visit http://www.ncbi.nlm.nih.gov/PubMed search menu should say PubMed type Neufeld TP in the avaliable line back to top |
||||||
|
|||||||
 |
 |
 |
|
||||
|
