Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 99, Issue 22, Pages 14315-14319Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.222531899
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Funding
- NIA NIH HHS [R03 AG020816, R37 AG016667, AG-20816, AG-14532] Funding Source: Medline
- NIDDK NIH HHS [DK-17433, R37 DK033793, R01 DK033793, P01 DK017433, DK-33793] Funding Source: Medline
- NIEHS NIH HHS [ES-11463] Funding Source: Medline
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Caloric restriction extends life span in a variety of species, highlighting the importance of energy balance in aging. A new longevity gene, Indy (for I'm not dead yet), which doubles the average life span of flies without a loss of fertility or physical activity, was postulated to extend life by affecting intermediary metabolism. We report that functional studies in Xenopus oocytes show INDY is a metabolite transporter that mediates the high-affinity, disulfonic stilbene-sensitive flux of dicarboxylates and citrate across the plasma membrane by a mechanism that is not coupled to Na+, K+, or Cl-. Immunocytochemical studies localize INDY to the plasma membrane with most prominent expression in adult fat body, oenocytes, and the basolateral region of midgut cells and show that life-extending mutations in Indy reduce INDY expression. We conclude that INDY functions as a novel sodium-independent mechanism for transporting Krebs and citric acid cycle intermediates through the epithelium of the gut and across the plasma membranes of organs involved in intermediary metabolism and storage. The life-extending effect of mutations in Indy is likely caused by an alteration in energy balance caused by a decrease in INDY transport function.
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