Extension of Life-Span by Loss of CHICO, a Drosophila Insulin Receptor Substrate Protein

Authors

• David Clancy, University College London, Wolfson House, 4 Stephenson Way, London
• David Gems, University College London, Wolfson House, 4 Stephenson Way, London
• Lawrence G. Harshman, University of Nebraska - LincolnFollow
• Sean Oldham, Universität Zürich, Winterthurerstrasse 190, 8057 Zürich, Switzerland
• Hugo Stocker, Universität Zürich, Winterthurerstrasse 190, 8057 Zürich, Switzerland
• Ernest Hafen, Universität Zürich, Winterthurerstrasse 190, 8057 Zürich, Switzerland
• Sally Leevers, Ludwig Institute for Cancer Research, 91 Riding House Street, London W1W 7BS, UK
• Linda Partridge, University College London, Wolfson House, 4 Stephenson Way, London

Document Type

Article

Date of this Version

4-6-2001

Comments

Published in Science 292 (April 6, 2001), pp. 104–106; doi 10.1126/science.1057991 Copyright © 2001 American Association for the Advancement of Science. Used by permission. http://www.sciencemag.org/cgi/content/full/292/5514/104

Abstract

The Drosophila melanogaster gene chico encodes an insulin receptor substrate that functions in an insulin/insulin-like growth factor (IGF) signaling pathway. In the nematode Caenorhabditis elegans, insulin/IGF signaling regulates adult longevity. We found that mutation of chico extends fruit fl y median life-span by up to 48% in homozygotes and 36% in heterozygotes. Extension of life-span was not a result of impaired oogenesis in chico females, nor was it consistently correlated with increased stress resistance. The dwarf phenotype of chico homozygotes was also unnecessary for extension of life-span. The role of insulin/IGF signaling in regulating animal aging is therefore evolutionarily conserved.