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Scott Kennedy

Assistant Professor of Pharmacology

Address:

2434 Genetics/Biotech

Telephone:

890-0227

Email:

sgkennedy@wisc.edu

Research Fields:

C. elegans

Molecular Genetics

Genomics

Research Interests

Molecular understanding of small RNAs

Research Description

Small RNAs of 21-24 nucleotides in length function in a remarkably wide range of biological processes, including gene silencing, translational regulation, heterochromatin formation, developmental timing, antiviral defense, and genome rearrangement. The long-term interest of my laboratory is to gain a molecular understanding of the endogenous biological functions of small RNAs. In particular, we are interested in the evolutionarily conserved process of RNA interference (RNAi). Exposure of many organisms to double-stranded (ds) RNA causes the degradation of mRNA molecules containing sequences homologous to the trigger dsRNA. dsRNAs are processed by the RNase III enzyme Dicer (DCR-1) into small RNAs [termed small interfering RNAs (siRNAs)] which hybridize to and induce the degradation of cognate mRNAs. This gene-silencing phenomenon has been termed RNA interference (RNAi).

We are undertaking genetic screens in the model organism C. elegans to identify and characterize the RNAi machinery. These screens are targeting genes that are required for appropriate organismal responses to dsRNA and genes which function to negatively regulate RNAi. An additional goal of the laboratory is to further our understanding of the endogenous biological functions of this conserved RNAi machinery. Several possibilities for these functions include: protecting organisms from parasitic nucleic acids such as viruses and transposons, the regulation of transcription and chromatin structure, and the post-transcriptional regulation of cellular mRNAs. We are using genetics, molecular biology, and biochemistry to answer these questions.

Much of the RNAi machinery is conserved in mammals, indicating that research on RNAi in model organisms such as C. elegans will not only be fundamental to our understanding of the biology of RNAi, but also instrumental in the rational use of RNAi technology in mammalian systems, and in the use of RNAi as a possible therapeutic to treat human disease.

Representative Publications

• Duchaine T., Wohlschlegel, J., Kennedy S., Bei Y., Conte D., Pang K., Brownell D., Harding S., Mitani S., Ruvkun G., Yates J. and Mello C. 2006. Functional Proteomics Reveals the Biochemical Niche of C. elegans DCR-1 in Multiple small-RNA-mediated Pathways. Cell. In Press.
• Wang D., Kennedy S., Conte D., Kim J., Gabel H., Kamath R., Mello C. and Ruvkun G. 2005. Somatic misexpression of germline P granules and enhanced RNA interference in C. elegans retinoblastoma pathway mutants. Nature. 436: 593-597.
• Kennedy, S., Wang D. and G. Ruvkun. 2004. A conserved siRNA-degrading RNase negatively regulates RNA interference in C. elegans. Nature. 427:645-9.
• Lee, S.S., Kennedy, S., Tolonen, A.C. and G. Ruvkun. 2003. DAF-16 target genes that control C. elegans life-span and metabolism. Science. 300:644-7.
• Kennedy, S.G., Wagner, A.J., Conzen, S.D., Jordan, J., Bellacosa, A., Tsichlis, PN. and Hay, N. 1997. The PI 3-Kinase/Akt Signaling Pathway Delivers an Anti-Apoptotic Signal. Genes Dev. 11:701-713.