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Human Molecular Genetics Advance Access published online on June 18, 2007
Human Molecular Genetics, doi:10.1093/hmg/ddm143
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© The Author 2007. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

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, University of Washington, Seattle, WA 98104, USA 3 Division of Neurogenetics, Department of Neurology, University of Washington, Seattle WA, 98104 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, Phone (206) 277-3275, Fax (206) 764-2569 Email: kraemerb{at}u.washington.edu

Received March 29, 2007; Revised May 29, 2007; Accepted May 29, 2007

We previously reported a transgenic C. 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 tauinduced phenotype. Thus, we have found a conserved molecular pathway participating in tau neurotoxicity in C. elegans.


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