Tags

Type your tag names separated by a space and hit enter

Nicotinamide adenine dinucleotide extends the lifespan of Caenorhabditis elegans mediated by sir-2.1 and daf-16.
Biogerontology 2010; 11(1):31-43B

Abstract

It is well understood that sir2 (sirtuin), an NAD-dependent deacetylase, is essential for the extension of lifespan under caloric restriction. However, the mechanism underlying activation of sir2 is unclear. Life extension through caloric restriction requires the sir2 ortholog sir-2.1 in nematodes but occurs independently of the forkhead-type transcription factor DAF-16. We aimed here to elucidate the correlation between life extension in nematodes and NAD-dependent activation of sirtuin by analyzing the relationship between NAD and DAF-16. Lifespan was extended when Caenorhabditis elegans were bred using medium containing NAD. An RNA interference experiment revealed that life extension by NAD was sir-2.1 dependent. However, life extension by NAD did not occur in daf-16-RNAi nematodes, suggesting that NAD-dependent longevity requires daf-16. This result suggested that different signaling pathways are involved in life extension resulting from caloric restriction and from NAD addition. Expression of sod-3, a target gene of daf-16, and increased oxidative-stress resistance and adiposity were observed in response to NAD addition, indicating that NAD activated daf-16 in each phenotype. These results suggest that NAD affected lifespan through the activation of SIR-2.1 and DAF-16 along a signaling pathway, namely insulin-like signalling pathway (at least parts of it), different from that associated with caloric restriction.

Authors+Show Affiliations

Graduate School of Life and Environmental Sciences, University of Tsukuba, 1-1-1 Tennoudai, Tsukuba, Ibaraki, Japan.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

19370397

Citation

Hashimoto, Teppei, et al. "Nicotinamide Adenine Dinucleotide Extends the Lifespan of Caenorhabditis Elegans Mediated By Sir-2.1 and Daf-16." Biogerontology, vol. 11, no. 1, 2010, pp. 31-43.
Hashimoto T, Horikawa M, Nomura T, et al. Nicotinamide adenine dinucleotide extends the lifespan of Caenorhabditis elegans mediated by sir-2.1 and daf-16. Biogerontology. 2010;11(1):31-43.
Hashimoto, T., Horikawa, M., Nomura, T., & Sakamoto, K. (2010). Nicotinamide adenine dinucleotide extends the lifespan of Caenorhabditis elegans mediated by sir-2.1 and daf-16. Biogerontology, 11(1), pp. 31-43. doi:10.1007/s10522-009-9225-3.
Hashimoto T, et al. Nicotinamide Adenine Dinucleotide Extends the Lifespan of Caenorhabditis Elegans Mediated By Sir-2.1 and Daf-16. Biogerontology. 2010;11(1):31-43. PubMed PMID: 19370397.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Nicotinamide adenine dinucleotide extends the lifespan of Caenorhabditis elegans mediated by sir-2.1 and daf-16. AU - Hashimoto,Teppei, AU - Horikawa,Makoto, AU - Nomura,Toshihisa, AU - Sakamoto,Kazuichi, Y1 - 2009/04/16/ PY - 2009/01/05/received PY - 2009/04/02/accepted PY - 2009/4/17/entrez PY - 2009/4/17/pubmed PY - 2010/3/11/medline SP - 31 EP - 43 JF - Biogerontology JO - Biogerontology VL - 11 IS - 1 N2 - It is well understood that sir2 (sirtuin), an NAD-dependent deacetylase, is essential for the extension of lifespan under caloric restriction. However, the mechanism underlying activation of sir2 is unclear. Life extension through caloric restriction requires the sir2 ortholog sir-2.1 in nematodes but occurs independently of the forkhead-type transcription factor DAF-16. We aimed here to elucidate the correlation between life extension in nematodes and NAD-dependent activation of sirtuin by analyzing the relationship between NAD and DAF-16. Lifespan was extended when Caenorhabditis elegans were bred using medium containing NAD. An RNA interference experiment revealed that life extension by NAD was sir-2.1 dependent. However, life extension by NAD did not occur in daf-16-RNAi nematodes, suggesting that NAD-dependent longevity requires daf-16. This result suggested that different signaling pathways are involved in life extension resulting from caloric restriction and from NAD addition. Expression of sod-3, a target gene of daf-16, and increased oxidative-stress resistance and adiposity were observed in response to NAD addition, indicating that NAD activated daf-16 in each phenotype. These results suggest that NAD affected lifespan through the activation of SIR-2.1 and DAF-16 along a signaling pathway, namely insulin-like signalling pathway (at least parts of it), different from that associated with caloric restriction. SN - 1573-6768 UR - https://www.unboundmedicine.com/medline/citation/19370397/Nicotinamide_adenine_dinucleotide_extends_the_lifespan_of_Caenorhabditis_elegans_mediated_by_sir_2_1_and_daf_16_ L2 - https://doi.org/10.1007/s10522-009-9225-3 DB - PRIME DP - Unbound Medicine ER -