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Multiple pathways regulating the calorie restriction response in yeast.(Author abstract)(Report)

In yeast, SIR2 overexpression or calorie restriction (CR) results in life-span extension. It was previously suggested that CR activates Sir2 by reducing the levels of Sir2 inhibitors, NADH, or nicotinamide. Whereas NADH reduction is associated with an increase in respiration, nicotinamide clearance... Full description

Journal Title: The Journals of Gerontology Series A, Feb, 2011, Vol.66(2), p.163(7)
Main Author: Rahat, Ofer
Other Authors: Maoz, Noam , Cohen, Haim Y.
Format: Electronic Article Electronic Article
Language: English
Subjects:
ID: ISSN: 1079-5006
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recordid: gale_ofa248733719
title: Multiple pathways regulating the calorie restriction response in yeast.(Author abstract)(Report)
format: Article
creator:
  • Rahat, Ofer
  • Maoz, Noam
  • Cohen, Haim Y.
subjects:
  • Low Calorie Diet -- Research
  • Life Span (Biology) -- Research
  • Genetic Research
ispartof: The Journals of Gerontology, Series A, Feb, 2011, Vol.66(2), p.163(7)
description: In yeast, SIR2 overexpression or calorie restriction (CR) results in life-span extension. It was previously suggested that CR activates Sir2 by reducing the levels of Sir2 inhibitors, NADH, or nicotinamide. Whereas NADH reduction is associated with an increase in respiration, nicotinamide clearance is induced by the upregulation of PNC1. Here, we show that, consistent with the hormesis hypothesis, PNC1 is part of a transcriptional stress response module consisting of 39 genes that increases under various stresses. Under high CR (0.1% glucose), Pnc1 becomes activated and its levels increase. However, low CR (0.5% glucose) increases yeast life span without PNC1 induction or activation of any transcriptional stress response. Instead, microarray analysis of low CR shows that the messenger RNA levels of iron transport genes increase, suggesting that this mode of CR is regulated by a shift toward respiration and lowering NADH levels. Thus, at least two pathways regulate the CR response in yeast. Key Words: Calorie restriction--Respiration--Stress--Yeast. Received May 18, 2010; Accepted August 28, 2010 Decision Editor: Rafael de Cabo, PhD doi: 10.1093/gerona/glq165
language: English
source:
identifier: ISSN: 1079-5006
fulltext: fulltext
issn:
  • 1079-5006
  • 10795006
url: Link


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titleMultiple pathways regulating the calorie restriction response in yeast.(Author abstract)(Report)
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subjectLow Calorie Diet -- Research ; Life Span (Biology) -- Research ; Genetic Research
descriptionIn yeast, SIR2 overexpression or calorie restriction (CR) results in life-span extension. It was previously suggested that CR activates Sir2 by reducing the levels of Sir2 inhibitors, NADH, or nicotinamide. Whereas NADH reduction is associated with an increase in respiration, nicotinamide clearance is induced by the upregulation of PNC1. Here, we show that, consistent with the hormesis hypothesis, PNC1 is part of a transcriptional stress response module consisting of 39 genes that increases under various stresses. Under high CR (0.1% glucose), Pnc1 becomes activated and its levels increase. However, low CR (0.5% glucose) increases yeast life span without PNC1 induction or activation of any transcriptional stress response. Instead, microarray analysis of low CR shows that the messenger RNA levels of iron transport genes increase, suggesting that this mode of CR is regulated by a shift toward respiration and lowering NADH levels. Thus, at least two pathways regulate the CR response in yeast. Key Words: Calorie restriction--Respiration--Stress--Yeast. Received May 18, 2010; Accepted August 28, 2010 Decision Editor: Rafael de Cabo, PhD doi: 10.1093/gerona/glq165
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titleMultiple pathways regulating the calorie restriction response in yeast.(Author abstract)(Report)
descriptionIn yeast, SIR2 overexpression or calorie restriction (CR) results in life-span extension. It was previously suggested that CR activates Sir2 by reducing the levels of Sir2 inhibitors, NADH, or nicotinamide. Whereas NADH reduction is associated with an increase in respiration, nicotinamide clearance is induced by the upregulation of PNC1. Here, we show that, consistent with the hormesis hypothesis, PNC1 is part of a transcriptional stress response module consisting of 39 genes that increases under various stresses. Under high CR (0.1% glucose), Pnc1 becomes activated and its levels increase. However, low CR (0.5% glucose) increases yeast life span without PNC1 induction or activation of any transcriptional stress response. Instead, microarray analysis of low CR shows that the messenger RNA levels of iron transport genes increase, suggesting that this mode of CR is regulated by a shift toward respiration and lowering NADH levels. Thus, at least two pathways regulate the CR response in yeast. Key Words: Calorie restriction--Respiration--Stress--Yeast. Received May 18, 2010; Accepted August 28, 2010 Decision Editor: Rafael de Cabo, PhD doi: 10.1093/gerona/glq165
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abstractIn yeast, SIR2 overexpression or calorie restriction (CR) results in life-span extension. It was previously suggested that CR activates Sir2 by reducing the levels of Sir2 inhibitors, NADH, or nicotinamide. Whereas NADH reduction is associated with an increase in respiration, nicotinamide clearance is induced by the upregulation of PNC1. Here, we show that, consistent with the hormesis hypothesis, PNC1 is part of a transcriptional stress response module consisting of 39 genes that increases under various stresses. Under high CR (0.1% glucose), Pnc1 becomes activated and its levels increase. However, low CR (0.5% glucose) increases yeast life span without PNC1 induction or activation of any transcriptional stress response. Instead, microarray analysis of low CR shows that the messenger RNA levels of iron transport genes increase, suggesting that this mode of CR is regulated by a shift toward respiration and lowering NADH levels. Thus, at least two pathways regulate the CR response in yeast. Key Words: Calorie restriction--Respiration--Stress--Yeast. Received May 18, 2010; Accepted August 28, 2010 Decision Editor: Rafael de Cabo, PhD doi: 10.1093/gerona/glq165
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