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Research Paper|Volume 5, Issue 9|pp 662—681

Increased longevity mediated by yeast NDI1 expression in Drosophila intestinal stem and progenitor cells

Jae H. Hur1, Sepehr Bahadorani1, Jacqueline Graniel1, Christopher L. Koehler2,3, Matthew Ulgherait1, Michael Rera1, D. Leanne Jones2,3, David W. Walker1,4
  • 1Department of Integrative Biology and Physiology, University of California, Los Angeles, Los Angeles, CA 90095, USA
  • 2Laboratory of Genetics, The Salk Institute for Biological Studies, La Jolla, CA 92037, USA
  • 3Department of Molecular, Cell and Developmental Biology, University of California, Los Angeles, Los Angeles, CA 90095, USA
  • 4Molecular Biology Institute, University of California, Los Angeles, Los Angeles, CA 90095, USA
Received: August 27, 2013Accepted: September 5, 2013Published: September 6, 2013
https://doi.org/10.18632/aging.100595

Copyright: © 2013 Hur et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

A functional decline in tissue stem cells and mitochondrial dysfunction have each been linked to aging and multiple aging-associated pathologies. However, the interplay between energy homeostasis, stem cells, and organismal aging remains poorly understood. Here, we report that expression of the single-subunit yeast alternative NADH dehydrogenase, ndi1, in Drosophila intestinal stem and progenitor cells delays the onset of multiple markers of intestinal aging and extends lifespan. In addition, expression of ndi1 in the intestine increases feeding behavior and results in organismal weight gain. Consistent with increased nutrient uptake, flies expressing ndi1 in the digestive tract display a systemic reduction in the activity of AMP-activated protein kinase (AMPK), a key cellular energy sensor. Together, these results demonstrate that ndi1 expression in the intestinal epithelium is an effective strategy to delay tissue and organismal aging.