Feeding Drosophila a biotin-deficient diet for multiple generations increases stress resistance and lifespan and alters gene expression and histone biotinylation patterns

Authors

Erin M. Smith, University of Nebraska-LincolnFollow
Jia Tse Hoi, University of Nebraska-Lincoln
Joel C. Eissenberg, Saint Louis University School of Medicine
James D. Shoemaker, Saint Louis University School of Medicine
Wendi S. Neckameyer, Saint Louis University School of Medicine
Anne M. Ilvarsonn, Saint Louis University School of Medicine
Lawrence G. Harshman, University of Nebraska-LincolnFollow
Vicki L. Schlegel, University of Nebraska - LincolnFollow
Janos Zempleni, University of Nebraska-LincolnFollow

Document Type

Article

Date of this Version

2007

Citation

J Nutr. 2007 September ; 137(9): 2006–2012.

Comments

© American Society for Nutrition

Abstract

Caloric restriction increases stress resistance and lifespan in Drosophila melanogaster and other species. The roles of individual nutrients in stress resistance and longevity are largely unknown. The vitamin biotin is a potential candidate for mediating these effects, given its known roles in stress signaling and gene regulation by epigenetic mechanisms, i.e., biotinylation of histones. Here, we tested the hypothesis that prolonged culture of Drosophila on biotin-deficient medium increases stress resistance and lifespan. Flies were fed a biotin-deficient diet for multiple generations; controls were fed a biotin-normal diet. In some experiments, a third group of flies was fed a biotin-deficient diet for 12 generations and then switched to control diets for two generations to eliminate potential effects of short-term biotin deficiency. Flies fed a biotin-deficient diet exhibited a 30% increase in lifespan. This increase was associated with enhanced resistance to the DNA-damaging agent hydroxyurea and heat stress. Also, fertility increased significantly compared with biotin-normal controls. Biotinylation of histones was barely detectable in biotin-deprived flies, suggesting that epigenetic events might have contributed to effects of biotin deprivation.