The general control nonderepressible-2 kinase mediates stress response and longevity induced by target of rapamycin inactivation in Caenorhabditis elegans
Article first published online: 28 JUN 2013
© 2013 The Authors. Aging Cell published by the Anatomical Society and John Wiley & Sons Ltd.
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Volume 12, Issue 5, pages 742–751, October 2013
How to Cite
Rousakis, A., Vlassis, A., Vlanti, A., Patera, S., Thireos, G. and Syntichaki, P. (2013), The general control nonderepressible-2 kinase mediates stress response and longevity induced by target of rapamycin inactivation in Caenorhabditis elegans. Aging Cell, 12: 742–751. doi: 10.1111/acel.12101
- Issue published online: 11 SEP 2013
- Article first published online: 28 JUN 2013
- Accepted manuscript online: 20 MAY 2013 09:16AM EST
- Manuscript Accepted: 8 APR 2013
- European Research Council. Grant Number: FP/2007-2013
- ERC. Grant Number: 201975
Fig. S1 Inactivation of leucyl-tRNA synthetase lrs-1 induces phospho-eIF2α levels in a gcn-2-dependent manner.
Fig. S2 Induction of atf-5::gfp transgene by eIF2α(RNAi) or tunicamycin does not require GCN-2 activity.
Fig S3 gcn-2 deletion does not alter fertility in wild-type or eat-2 mutants.
Fig. S4 Loss of GCN-2 activity sensitizes animals to amino acid limitation.
Fig. S5. RNAi efficiency is not affected in gcn-2 mutant worms.
Fig. S6 GCN-2 regulates the induction of PHA-4 target genes in eat-2 mutants.
Fig. S7 Inactivation of gcn-2 affects the induction of a Ppha-4::gfp reporter under oxidative stress.
Fig. S8 Loss of gcn-2 but not atf-5 increases the stress sensitivity of worms.
Table S1 List of the strains used in this study.
Table S2 List of primers used for plasmid construction in this study.
Table S3 Summary of data from independent repeats of lifespan experiments.
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