Deep sequencing of endogenous mRNA from Caenorhabditis elegans in the presence and absence of 1-methylnicotinamide (MNA) and nicotinic acid (NA)

ABSTRACT: Sirtuins, a family of histone deacetylases, have a fiercely debated role in regulating lifespan of different species. Contrasting recent observations, we here find that overexpression of sir-2.1, the orthologue of mammalian SirT1, does extend C. elegans lifespan. Sirtuins are known to convert NAD+ into nicotinamide (NAM). We here find that NAM and its metabolite, 1-methylnicotinamide (MNA), extend C. elegans lifespan, also in the absence of sir-2.1. Consistently, impairment of sir-2.1 prevents extension of lifespan by nicotinic acid (NA), a NAD+ precursor. Taken together, sirtuins extend lifespan by promoting formation of MNA to generate a phase I - mediated ROS signal, providing an unexpected mechanistic role for sirtuins beyond histone deacetylation. 9 samples: 3 mRNA profiles of C.elega

ORGANISM(S): Caenorhabditis elegans

SUBMITTER: Steffen Priebe 

PROVIDER: E-GEOD-49662 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress