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LET-60 RAS modulates effects of insulin/IGF-1 signaling on development and aging in Caenorhabditis elegans

LET-60 RAS modulates effects of insulin/IGF-1 signaling on development and aging in Caenorhabditis elegans
LET-60 RAS modulates effects of insulin/IGF-1 signaling on development and aging in Caenorhabditis elegans
The DAF-2 insulin/insulin-like growth factor 1 (IGF-1) receptor signals via a phosphatidylinositol 3-kinase (PI3K) pathway to control dauer larva formation and adult longevity in Caenorhabditis elegans. Yet epistasis analysis suggests signal bifurcation downstream of DAF-2. We have used epistasis analysis to test whether the Ras pathway (which plays a role in signaling from mammalian insulin receptors) acts downstream of DAF-2. We find that an activated Ras mutation, let-60(n1046gf), weakly suppresses constitutive dauer diapause in daf-2 and age-1 (PI3K) mutants. Moreover, increased Ras pathway signaling partially suppresses the daf-2 mutant feeding defect, while reduced Ras pathway signaling enhances it. By contrast, activated Ras extends the longevity induced by mutation of daf-2, while reduced Ras pathway signaling partially suppresses it. Thus, Ras pathway signaling appears to act with insulin/IGF-1 signaling during larval development, but against it during aging.
ageing, c.elegans, dauer larva, insulin/IGF-1 signalling, let-60/Ras
1474-9718
235-245
Nanji, Manoj
aa44af18-3422-4737-a644-8b727b1c1b40
Hopper, Neil A.
d2aed184-733b-47f6-8d74-fa1633ae6cf0
Gems, David
64f30241-6dab-4b23-af36-1e321fd317e7
Nanji, Manoj
aa44af18-3422-4737-a644-8b727b1c1b40
Hopper, Neil A.
d2aed184-733b-47f6-8d74-fa1633ae6cf0
Gems, David
64f30241-6dab-4b23-af36-1e321fd317e7

Nanji, Manoj, Hopper, Neil A. and Gems, David (2005) LET-60 RAS modulates effects of insulin/IGF-1 signaling on development and aging in Caenorhabditis elegans. Aging Cell, 4 (5), 235-245. (doi:10.1111/j.1474-9726.2005.00166.x).

Record type: Article

Abstract

The DAF-2 insulin/insulin-like growth factor 1 (IGF-1) receptor signals via a phosphatidylinositol 3-kinase (PI3K) pathway to control dauer larva formation and adult longevity in Caenorhabditis elegans. Yet epistasis analysis suggests signal bifurcation downstream of DAF-2. We have used epistasis analysis to test whether the Ras pathway (which plays a role in signaling from mammalian insulin receptors) acts downstream of DAF-2. We find that an activated Ras mutation, let-60(n1046gf), weakly suppresses constitutive dauer diapause in daf-2 and age-1 (PI3K) mutants. Moreover, increased Ras pathway signaling partially suppresses the daf-2 mutant feeding defect, while reduced Ras pathway signaling enhances it. By contrast, activated Ras extends the longevity induced by mutation of daf-2, while reduced Ras pathway signaling partially suppresses it. Thus, Ras pathway signaling appears to act with insulin/IGF-1 signaling during larval development, but against it during aging.

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More information

Published date: October 2005
Keywords: ageing, c.elegans, dauer larva, insulin/IGF-1 signalling, let-60/Ras

Identifiers

Local EPrints ID: 32814
URI: https://eprints.soton.ac.uk/id/eprint/32814
ISSN: 1474-9718
PURE UUID: 2e765bd8-ffe8-4866-b960-1ca0bb35a349

Catalogue record

Date deposited: 12 May 2006
Last modified: 15 Jul 2019 19:07

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