These authors contributed equally to this work.
Molecular mechanisms underlying genotype-dependent responses to dietary restriction
Article first published online: 11 AUG 2013
© 2013 the Anatomical Society and John Wiley & Sons Ltd
Volume 12, Issue 6, pages 1050–1061, December 2013
How to Cite
Schleit, J., Johnson, S. C., Bennett, C. F., Simko, M., Trongtham, N., Castanza, A., Hsieh, E. J., Moller, R. M., Wasko, B. M., Delaney, J. R., Sutphin, G. L., Carr, D., Murakami, C. J., Tocchi, A., Xian, B., Chen, W., Yu, T., Goswami, S., Higgins, S., Jeong, K.-S., Kim, J. R., Klum, S., Liao, E., Lin, M. S., Lo, W., Miller, H., Olsen, B., Peng, Z. J., Pollard, T., Pradeep, P., Pruett, D., Rai, D., Ros, V., Singh, M., Spector, B. L., Wende, H. V., An, E. H., Fletcher, M., Jelic, M., Rabinovitch, P. S., MacCoss, M. J., Han, J.-D. J., Kennedy, B. K. and Kaeberlein, M. (2013), Molecular mechanisms underlying genotype-dependent responses to dietary restriction. Aging Cell, 12: 1050–1061. doi: 10.1111/acel.12130
- Issue published online: 21 NOV 2013
- Article first published online: 11 AUG 2013
- Accepted manuscript online: 10 JUL 2013 02:30AM EST
- Manuscript Accepted: 26 JUN 2013
- NIH. Grant Number: R01AG039390
- NIH Training. Grant Numbers: T32AG000057, T32ES007032, T32GM07270
- NIH. Grant Numbers: P30AG013280, P41GM103533
Fig. S1 Absolute changes in RLS among Single Gene Mutants on DR.
Fig. S2 AMIGO Visualization of GO Pathways Significantly Enriched in Mutants with RLS Significantly Decreased by DR.
Fig. S3 AMIGO Visualization of Molecular Function Groups Significantly Enriched in Mutants with RLS Significantly Decreased by DR.
Fig. S4 AMIGO Visualization of GO Pathways Significantly Enriched in Mutants with RLS Significantly Increased by DR.
Fig. S5 Additional Dose-Response Profiles of Selected Single Gene Mutants on DR.
Fig. S6 RLS of wild-type and single mutant strains on 2% glucose and DR conditions.
Fig. S7 Prohibitin deficient cells have altered mitochondrial membrane potential.
Fig. S8 Inhibition of respiration prevents growth of phbΔ cells on non-fermentable carbon sources.
Fig. S9 Proteomic analysis reveals expected changes to respiratory proteins on DR as well as revealing the specificity of the induction of the mitochondrial unfolded protein response in phbΔ cells.
Fig. S10 P- and Q-value histograms of proteomic data.
Fig. S11 Properties of BY4742 and phbΔ cells lacking RPL20B, RPS7A, or SCH9.
Fig. S12 RNAi knockdown of PHB in C. elegans increases HSP-6 expression throughout their life span.
Fig. S13 RNAi knockdown of PHB in C. elegans does not induce the cytoplasmic- or endoplasmic reticulum -associated UPR.
Fig. S14 Prohibitin deficient cells display synthetic lethal inheritance patterns when crossed to strains lacking AFG3 or YTA12.
Fig. S15 DR shortens the RLS of sod1Δ cells.
Table S1 Life span data of 166 single deletion strains on 2% glucose and 0.05% glucose.
Table S2 Life spans of strains with statistically significant difference in RLS between 2% glucose and 0.05% glucose.
Table S3 GO Terms significantly enriched in single gene mutant set for decreased lifespan on DR (1 of 3).
Table S4 GO Terms significantly enriched in single gene mutant set for decreased lifespan on DR (2 of 3).
Table S5 GO Terms significantly enriched in single gene mutant set for decreased lifespan on DR (3 of 3).
Table S6 GO terms significantly enriched in single gene mutant set for positive response to DR.
Table S7 Mean Replicative Lifespans of BY4742, sod2Δ, phb1Δ, and phb2Δ on fermentable and non-fermentable carbon sources.
Table S8 Full genotype and RLS data of double mutant strains tested.
Table S9 Mean Replicative Lifespans of sod1Δ and sod2Δ on 2% glucose and 0.05% glucose medias with and without 6 mm N-acetylcysteine (NAC).
Table S10 Pooled Spectral Count Data from phb1Δ and phb2Δ cells compared to WT 6 Targets differing from WT in on 2% Glucose and rescued on 3% glycerol.
Table S11 Gene ontology (GO) analysis of statistically significant targets.
Table S12 C. elegans life span data. Animals lost to foraging were not included.
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