Cited by 319

The DOI matches its Crossref record; 3 of the 3 references it cites were found in a registry or an index.

eIF4E function in somatic cells modulates ageing in Caenorhabditis elegans

Syntichaki, Popi, Troulinaki, Kostoula, Tavernarakis, Nektarios·2007·Nature

Abstract

Regulation of protein synthesis is critical for cell growth and maintenance. Ageing in many organisms, including humans, is accompanied by marked alterations in both general and specific protein synthesis. Whether these alterations are simply a corollary of the ageing process or have a causative role in senescent decline remains unclear. An array of protein factors facilitates the tight control of messenger RNA translation initiation. The eukaryotic initiation factor 4E (eIF4E), which binds the 7-monomethyl guanosine cap at the 5' end of all nuclear mRNAs, is a principal regulator of protein synthesis. Here we show that loss of a specific eIF4E isoform (IFE-2) that functions in somatic tissues reduces global protein synthesis, protects from oxidative stress and extends lifespan in Caenorhabditis elegans. Lifespan extension is independent of the forkhead transcription factor DAF-16, which mediates the effects of the insulin-like signalling pathway on ageing. Furthermore, IFE-2 deficiency further extends the lifespan of long-lived age and daf nematode mutants. Similarly, lack of IFE-2 enhances the long-lived phenotype of clk and dietary-restricted eat mutant animals. Knockdown of target of rapamycin (TOR), a phosphatidylinositol kinase-related kinase that controls protein synthesis in response to nutrient cues, further increases the longevity of ife-2 mutants. Thus, signalling via eIF4E in the soma is a newly discovered pathway influencing ageing in C. elegans.

Overview

Integrity signals

Registry

Crossref · 10.1038/nature05603

Cites

3 of 3 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Verification

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • Genetic inhibition of mTORC1 or downstream pathways extends lifespan in yeast, worms, and flies.

    “Studies in yeast, worms and flies found that genetic inhibition of mTORC1 or signaling pathways downstream of mTORC1, including S6K and translation initiation factors, extends lifespan 5–11.”

    From Targeting the biology of aging with mTOR inhibitors (2023) · cites this paper as [10]

  • Experiments in model organisms have shown that deletion or knockdown of ribosomal subunits, S6K1, or translation initiation factors results in increased lifespan.

    “In agreement with such a model, experiments in model organisms have shown that deletion or knockdown of ribosomal subunits, S6K1, or translation initiation factors results in increased lifespan 6,10.”

    From Targeting the biology of aging with mTOR inhibitors (2023) · cites this paper as [10]

  • Studies in C. elegans have shown that the lifespan of worms lacking eIF4E can be further increased by knockdown of the gene encoding TOR.

    “Studies in C. elegans have shown that the lifespan of worms lacking eukaryotic translation initiation factor 4E (eIF4E), which are long-lived and have a global reduction in protein synthesis, can be still further increased by knockdown of the gene encoding TOR 10.”

    From Targeting the biology of aging with mTOR inhibitors (2023) · cites this paper as [10]

Citations

Cites

Flagged first, then by citations

Research works printed but not linked: 29

  1. Ward, W. F. The relentless effects of the aging process on protein turnover. Biogerontology 1, 195–199 (2000) · DOI
  2. Gebauer, F. & Hentze, M. W. Molecular mechanisms of translational control. Nature Rev. Mol. Cell Biol. 5, 827–835 (2004) · DOI · Paper page
  3. Gingras, A. C., Raught, B. & Sonenberg, N. eIF4 initiation factors: effectors of mRNA recruitment to ribosomes and regulators of translation. Annu. Rev. Biochem. 68, 913–963 (1999) · DOI
  4. Keiper, B. D. et al. Functional characterization of five eIF4E isoforms in Caenorhabditis elegans. J. Biol. Chem. 275, 10590–10596 (2000) · DOI
  5. Amiri, A. et al. An isoform of eIF4E is a component of germ granules and is required for spermatogenesis in C. elegans. Development 128, 3899–3912 (2001) · DOI
  6. Beanan, M. J. & Strome, S. Characterization of a germ-line proliferation mutation in C. elegans. Development 116, 755–766 (1992) · DOI
  7. Lakowski, B. & Hekimi, S. Determination of life-span in Caenorhabditis elegans by four clock genes. Science 272, 1010–1013 (1996) · DOI
  8. Lakowski, B. & Hekimi, S. The genetics of caloric restriction in Caenorhabditis elegans. Proc. Natl Acad. Sci. USA 95, 13091–13096 (1998) · DOI
  9. Waskiewicz, A. J. et al. Phosphorylation of the cap-binding protein eukaryotic translation initiation factor 4E by protein kinase Mnk1 in vivo. Mol. Cell. Biol. 19, 1871–1880 (1999) · DOI
  10. Ruvinsky, I. & Meyuhas, O. Ribosomal protein S6 phosphorylation: from protein synthesis to cell size. Trends Biochem. Sci. 31, 342–348 (2006) · DOI
  11. Arquier, N., Bourouis, M., Colombani, J. & Leopold, P. Drosophila Lk6 kinase controls phosphorylation of eukaryotic translation initiation factor 4E and promotes normal growth and development. Curr. Biol. 15, 19–23 (2005) · DOI
  12. Reiling, J. H., Doepfner, K. T., Hafen, E. & Stocker, H. Diet-dependent effects of the Drosophila Mnk1/Mnk2 homolog Lk6 on growth via eIF4E. Curr. Biol. 15, 24–30 (2005) · DOI
  13. Jia, K., Chen, D. & Riddle, D. L. The TOR pathway interacts with the insulin signaling pathway to regulate C. elegans larval development, metabolism and life span. Development 131, 3897–3906 (2004) · DOI · Paper page
  14. Proud, C. G. Regulation of mammalian translation factors by nutrients. Eur. J. Biochem. 269, 5338–5349 (2002) · DOI
  15. Martin, G. M., Austad, S. N. & Johnson, T. E. Genetic analysis of ageing: role of oxidative damage and environmental stresses. Nature Genet. 13, 25–34 (1996) · DOI
  16. Stadtman, E. R. Protein oxidation and aging. Science 257, 1220–1224 (1992) · DOI
  17. Lin, S. J. & Culotta, V. C. The ATX1 gene of Saccharomyces cerevisiae encodes a small metal homeostasis factor that protects cells against reactive oxygen toxicity. Proc. Natl Acad. Sci. USA 92, 3784–3788 (1995) · DOI
  18. Yoshikawa, S. et al. Redox-coupled crystal structural changes in bovine heart cytochrome c oxidase. Science 280, 1723–1729 (1998) · DOI
  19. Vanfleteren, J. R. Oxidative stress and ageing in Caenorhabditis elegans. Biochem. J. 292, 605–608 (1993) · DOI
  20. Sohal, R. S. & Weindruch, R. Oxidative stress, caloric restriction, and aging. Science 273, 59–63 (1996) · DOI
  21. Tavernarakis, N., Wang, S. L., Dorovkov, M., Ryazanov, A. & Driscoll, M. Heritable and inducible genetic interference by double-stranded RNA encoded by transgenes. Nature Genet. 24, 180–183 (2000) · DOI
  22. Makrides, S. C. Protein synthesis and degradation during aging and senescence. Biol. Rev. Camb. Philos. Soc. 58, 343–422 (1983) · DOI
  23. Rattan, S. I. Synthesis, modifications, and turnover of proteins during aging. Exp. Gerontol. 31, 33–47 (1996) · DOI
  24. Tavernarakis, N. & Driscoll, M. Caloric restriction and lifespan: a role for protein turnover? Mech. Ageing Dev. 123, 215–229 (2002) · DOI
  25. Ruggero, D. et al. The translation factor eIF-4E promotes tumor formation and cooperates with c-Myc in lymphomagenesis. Nature Med. 10, 484–486 (2004) · DOI
  26. Ahmed, S. & Hodgkin, J. MRT-2 checkpoint protein is required for germline immortality and telomere replication in C. elegans. Nature 403, 159–164 (2000) · DOI
  27. Kirkwood, T. B. & Austad, S. N. Why do we age? Nature 408, 233–238 (2000) · DOI · Paper page
  28. Pan, K. Z. et al. Inhibition of mRNA translation extends lifespan in C. elegans. Ageing Cell doi:10.1111/j.1474-9726.2006.00266.x (5 December 2006). · DOI
  29. Hansen, M. et al. Lifespan extension by conditions that inhibit translation in C. elegans. Ageing Cell doi:10.1111/j.1474-9726.2006.00267.x (5 December 2006). · DOI · Paper page

Cited by

Sorted by citations

Metadata

Authors
Syntichaki, P., Troulinaki, K., & Tavernarakis, N.
Venue
Nature
Published
2007-02
Volume
445
Issue
7130
Pages
922-926
ISSN
  • 0028-0836
  • 1476-4687
Cited by
319
References
3
Language
en

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review