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Human Molecular Genetics Advance Access originally published online on June 18, 2007
Human Molecular Genetics 2007 16(16):1959-1971; doi:10.1093/hmg/ddm143
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Published by Oxford University Press 2007

SUT-1 enables tau-induced neurotoxicity in C. elegans

Brian C. Kraemer1,2,* and Gerard D. Schellenberg1,2,3,4

1 Geriatrics Research Education and Clinical Center, Veterans Affairs Puget Sound Health Care System, Seattle, WA 98108, USA, 2 Division of Gerontology and Geriatric Medicine, Department of Medicine, 3 Division of Neurogenetics, Department of Neurology and 4 Department of Pharmacology, University of Washington, Seattle, WA 98195, USA

* To whom correspondence should be addressed at:, Seattle Veterans Affairs Puget Sound Health Care System, S182, 1660 South Columbian Way, Seattle, WA 98108, USA. Tel: +1 2062773275; Fax: +1 2067642569; Email: kraemerb{at}u.washington.edu

Received March 29, 2007; Accepted June 3, 2007

We previously reported a transgenic Caenorhabditis elegans model for tauopathies in which expression of human tau in neurons caused insoluble phosphorylated tau accumulation, neurodegeneration and uncoordinated movement (Unc). To identify genes participating in tau neurotoxicity, we conducted a forward genetic screen for mutations that ameliorate tau-induced uncoordination. The recessive mutation sut-1(bk79) partially suppresses the Unc phenotype, tau aggregation and neurodegenerative changes caused by tau. We identified the sut-1 gene and found it encodes a novel protein. We conducted a yeast two hybrid screen to identify SUT-1 binding partners and found UNC-34, the C. elegans homolog of the cytoskeletal regulatory protein Enabled (ENA). In vitro protein binding assays and genetic studies validated the interaction between SUT-1 and UNC-34. The SUT-1/UNC-34 protein–protein interaction plays a role in both the normal function of UNC-34 and in the tau-induced phenotype. Thus, we have found a conserved molecular pathway participating in tau neurotoxicity in C. elegans.


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