Published March 10, 2000
| public
Journal Article
Genetic Suppression of Polyglutamine Toxicity in Drosophila
- Creators
- Kazemi-Esfarjani, Parsa
- Benzer, Seymour
Abstract
A Drosophila model for Huntington's and other polyglutamine diseases was used to screen for genetic factors modifying the degeneration caused by expression of polyglutamine in the eye. Among 7000 P-element insertions, several suppressor strains were isolated, two of which led to the discovery of the suppressor genes described here. The predicted product of one, dHDJ1, is homologous to human heat shock protein 40/HDJ1. That of the second, dTPR2, is homologous to the human tetratricopeptide repeat protein 2. Each of these molecules contains a chaperone-related J domain. Their suppression of polyglutamine toxicity was verified in transgenic flies.
Additional Information
© 2000 American Association for the Advancement of Science. 2 November 1999; accepted 24 January 2000. We thank C. Q. Doe for the gift of prospero cDNA clone p139cAC1; L. Seroude for the transgenic vector; and V. Sapin, R. Young, and A. Gomez for invaluable technical support. Supported by a Cure HD Initiative postdoctoral fellowship from the Hereditary Disease Foundation and a grant from the Wills Foundation to P.K.-E. and by grants to S.B. from NSF, NIH, and the James G. Boswell Foundation.Additional details
- Eprint ID
- 51693
- Resolver ID
- CaltechAUTHORS:20141113-073055190
- Hereditary Disease Foundation
- Wills Foundation
- NSF
- NIH
- James G. Boswell Foundation
- Created
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2014-11-13Created from EPrint's datestamp field
- Updated
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2021-11-10Created from EPrint's last_modified field