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The TOR pathway interacts with the insulin signaling pathway to regulate C. elegans larval development, metabolism and life span

Jia, Kailiang, Chen, Di, Riddle, Donald L.·2004·Development

Abstract

The highly conserved target-of-rapamycin (TOR) protein kinases control cell growth in response to nutrients and growth factors. In mammals, TOR has been shown to interact with raptor to relay nutrient signals to downstream translation machinery. We report that in C. elegans, mutations in the genes encoding CeTOR and raptor result in dauer-like larval arrest, implying that CeTOR regulates dauer diapause. The daf-15 (raptor) and let-363 (CeTOR) mutants shift metabolism to accumulate fat, and raptor mutations extend adult life span. daf-15 transcription is regulated by DAF-16, a FOXO transcription factor that is in turn regulated by daf-2 insulin/IGF signaling. This is a new mechanism that regulates the TOR pathway. Thus, DAF-2 insulin/IGF signaling and nutrient signaling converge on DAF-15 (raptor) to regulate C. elegans larval development, metabolism and life span.

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Crossref · 10.1242/dev.01255

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  • Genetic or pharmacological inhibition of TOR signalling extends lifespan in invertebrates including yeast, nematodes and fruit flies.

    “Inhibition of the TOR signalling pathway by genetic or pharmacological intervention extends lifespan in invertebrates, including yeast, nematodes and fruit flies1–5.”
  • Initial evidence that reduced TOR function can extend longevity came primarily from studies in yeast and invertebrates.

    “Initial evidence that reduced TOR function can extend longevity came primarily from studies in yeast1,2 and invertebrates3–5.”

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Research works printed but not linked: 40

  1. Abraham, R. T. (2002). Identification of TOR signaling complexes: more TORC for the cell growth engine. Cell111,9-12. · DOI
  2. Albert, P. S. and Riddle, D. L. (1988). Mutants of Caenorhabditis elegans that form dauer-like larvae. Dev. Biol.126,270-293. · DOI
  3. Bergamini, E., Cavallini, G., Donati, A. and Gori, Z.(2003). The anti-ageing effects of caloric restriction may involve stimulation of macroautophagy and lysosomal degradation, and can be intensified pharmacologically. Biomed. Pharmacother.57,203-208. · DOI
  4. Brenner, S. (1974). The genetics of Caenorhabditis elegans.Genetics77, 71-94. · DOI
  5. Brunk, U. T. and Terman, A. (2002). The mitochondrial-lysosomal axis theory of aging: accumulation of damaged mitochondria as a result of imperfect autophagocytosis. Eur. J. Biochem.269,1996-2002. · DOI
  6. Chalfie, M., Tu, Y., Euskirchen, G., Ward, W. W. and Prasher, D. C. (1994). Green fluorescent protein as a marker for gene expression. Science263,802-805. · DOI · Paper page
  7. Chen, J., Zheng, X. F., Brown, E. J. and Schreiber, S. L.(1995). Identification of an 11-kDa FKBP12-rapamycin-binding domain within the 289-kDa FKBP12-rapamycin-associated protein and characterization of a critical serine residue. Proc. Natl. Acad. Sci. USA92,4947-4951. · DOI · Paper page
  8. Choi, J., Chen, J., Schreiber, S. L. and Clardy, J.(1996). Structure of the FKBP12-rapamycin complex interacting with the binding domain of human FRAP. Science273,239-242. · DOI
  9. Chomczynski, P. and Sacchi, N. (1987). Single-step method of RNA isolation by acid guanidinium thiocyanate-phenol-chloroform extraction. Anal. Biochem.162,156-159. · DOI
  10. Conlon, I. and Raff, M. (1999). Size control in animal development. Cell96,235-244. · DOI
  11. Fire, A., Xu, S., Montgomery, M. K., Kostas, S. A., Driver, S. E. and Mello, C. C. (1998). Potent and specific genetic interference by double-stranded RNA in Caenorhabditis elegans.Nature391,806-811. · DOI · Paper page
  12. Gems, D., Sutton, A. J., Sundermeyer, M. L., Albert, P. S.,King, K. V., Edgley, M. L., Larsen, P. L. and Riddle, D. L.(1998). Two pleiotropic classes of daf-2 mutation affect larval arrest, adult behavior, reproduction and longevity in Caenorhabditis elegans.Genetics150,129-155. · DOI
  13. Hara, K., Maruki, Y., Long, X., Yoshino, K., Oshiro, N.,Hidayat, S., Tokunaga, C., Avruch, J. and Yonezawa, K.(2002). Raptor, a binding partner of target of rapamycin (TOR),mediates TOR action. Cell110,177-189. · DOI
  14. Heitman, J., Movva, N. R. and Hall, M. N.(1991). Targets for cell cycle arrest by the immunosuppressant rapamycin in yeast. Science253,905-909. · DOI
  15. Huang, S. and Houghton, P. J. (2003). Targeting mTOR signaling for cancer therapy. Curr. Opin. Pharmacol.3,371-377. · DOI
  16. Kamath, R. S., Martinez-Campos, M., Zipperlen, P., Fraser, A. G. and Ahringer, J. (2000). Effectiveness of specific RNA-mediated interference through ingested double-stranded RNA in Caenorhabditis elegans.Genome Biol.2, 1-10. · DOI
  17. Kenyon, C. (1997). Environmental factors and gene activities that influence life span. In C. elegans II (ed. D. L. Riddle, T. Blumenthal, B. J. Meyer and J. R. Priess), pp. 791-813. New York, NY: Cold Spring Harbor Laboratory Press.
  18. Kim, D. H., Sarbassov, D. D., Ali, S. M., King, J. E., Latek, R. R., Erdjument-Bromage, H., Tempst, P. and Sabatini, D. M.(2002). mTOR interacts with raptor to form a nutrient-sensitive complex that signals to the cell growth machinery. Cell110,163-175. · DOI
  19. Kimura, K. D., Tissenbaum, H. A., Liu, Y. and Ruvkun, G.(1997). daf-2, an insulin receptor-like gene that regulates longevity and diapause in Caenorhabditis elegans.Science277,942-946. · DOI
  20. Klass, M. R. (1977). Ageing in the nematode Caenorhabditis elegans: major biological and environmental factors influencing life span. Mech. Ageing Dev.6, 413-429. · DOI
  21. Lakowski, B. and Hekimi, S. (1998). The genetics of caloric restriction in Caenorhabditis elegans.Proc. Natl. Acad. Sci. USA95,13091-13096. · DOI
  22. Larsen, P. L., Albert, P. S. and Riddle, D. L.(1995). Genes that regulate both development and longevity in Caenorhabditis elegans.Genetics139,1567-1583. · DOI
  23. Lin, K., Dorman, J. B., Rodan, A. and Kenyon, C.(1997). daf-16: an HNF-3/forkhead family member that can function to double the life-span of Caenorhabditis elegans.Science278,1319-1322. · DOI
  24. Melendez, A., Talloczy, Z., Seaman, M., Eskelinen, E. L., Hall,D. H. and Levine, B. (2003). Autophagy genes are essential for dauer development and life-span extension in C. elegans.Science301,1387-1391. · DOI · Paper page
  25. Morris, J. Z., Tissenbaum, H. A. and Ruvkun, G.(1996). A phosphatidylinositol-3-OH kinase family member regulating longevity and diapause in Caenorhabditis elegans.Nature382,536-539. · DOI
  26. Murphy, C. T., McCarroll, S. A., Bargmann, C. I., Fraser, A.,Kamath, R. S., Ahringer, J., Li, H. and Kenyon, C. (2003). Genes that act downstream of DAF-16 to influence the lifespan of Caenorhabditis elegans.Nature424,277-283. · DOI · Paper page
  27. Neshat, M. S., Mellinghoff, I. K., Tran, C., Stiles, B., Thomas,G., Petersen, R., Frost, P., Gibbons, J. J., Wu, H. and Sawyers, C. L.(2001). Enhanced sensitivity of PTEN-deficient tumors to inhibition of FRAP/mTOR. Proc. Natl. Acad. Sci. USA98,10314-10319. · DOI
  28. O'Brien, R. M., Streeper, R. S., Ayala, J. E., Stadelmaier, B. T. and Hornbuckle, L. A. (2001). Insulin-regulated gene expression. Biochem. Soc. Trans.29,552-558. · DOI
  29. Ogg, S., Paradis, S., Gottlieb, S., Patterson, G. I., Lee, L. Tissenbaum, H. A. and Ruvkun, G. (1997). The Fork head transcription factor DAF-16 transduces insulin-like metabolic and longevity signals in C. elegans.Nature389,994-999. · DOI
  30. Oldham, S. and Hafen, E. (2003). Insulin/IGF and target of rapamycin signaling: a TOR de force in growth control. Trends Cell Biol.13,79-85. · DOI
  31. Oldham, S., Montagne, J., Radimerski, T., Thomas, G. and Hafen,E. (2000). Genetic and biochemical characterization of dTOR,the Drosophila homolog of the target of rapamycin. Genes Dev.14,2689-2694. · DOI
  32. Podsypanina, K., Lee, R. T., Politis, C., Hennessy, I., Crane,A., Puc, J., Neshat, M., Wang, H., Yang, L., Gibbons, J. et al.(2001). An inhibitor of mTOR reduces neoplasia and normalizes p70/S6 kinase activity in Pten+/– mice. Proc. Natl. Acad. Sci. USA98,10320-10325. · DOI
  33. Puig, O., Marr, M. T., Ruhf, M. L. and Tjian, R.(2003). Control of cell number by Drosophila FOXO:downstream and feedback regulation of the insulin receptor pathway. Genes Dev.17,2006-2020. · DOI
  34. Riddle, D. L. and Albert, P. S. (1997). Genetic and environmental regulation of dauer larva development. In C. elegans II (ed. D. L. Riddle, T. Blumenthal, B. J. Meyer and J. R. Priess), pp. 739-768. New York, NY: Cold Spring Harbor Laboratory Press.
  35. Schmelzle, T. and Hall, M. N. (2000). TOR, a central controller of cell growth. Cell253,103-262. · DOI
  36. Stan, R., McLaughlin, M. M., Cafferkey, R., Johnson, R. K.,Rosenberg, M. and Livi, G. P. (1994). Interaction between FKBP12-rapamycin and TOR involves a conserved serine residue. J. Biol. Chem.269,32027-32030. · DOI
  37. Tatar, M., Kopelman, A., Epstein, D., Tu, M. P., Yin, C. M. and Garofalo, R. S. (2001). A mutant Drosophila insulin receptor homolog that extends life-span and impairs neuroendocrine function. Science292,107-110. · DOI
  38. Wedaman, K. P., Reinke, A., Anderson, S., Yates, J. III,McCaffery, J. M. and Powers, T. (2003). Tor kinases are in distinct membrane-associated protein complexes in Saccharomyces cerevisiae.Mol. Biol. Cell14,1204-1220. · DOI
  39. Wicks, S. R., Yeh, R. T., Gish, W. R., Waterston, R. H. and Plasterk, R. H. (2001). Rapid gene mapping in Caenorhabditis elegans using a high density polymorphism map. Nat. Genet.28,160-164. · DOI
  40. Zhang, H., Stallock, J. P., Ng, J. C., Reinhard, C. and Neufeld,T. P. (2000). Regulation of cellular growth by the Drosophila target of rapamycin dTOR. Genes Dev.14,2712-2724. · DOI

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Metadata

Authors
Jia, K., Chen, D., & Riddle, D. L.
Affiliations
Molecular Biology Program and Division of Biological Sciences, University of Missouri, Columbia, MO 65211, USA
Venue
Development
Published
2004-08-15
Volume
131
Issue
16
Pages
3897-3906
ISSN
  • 1477-9129
  • 0950-1991
Cited by
615
References
3
Language
en

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