Disruption of Snf3/Rgt2 glucose sensors decreases lifespan and caloric restriction effectiveness through Mth1/Std1 by adjusting mitochondrial efficiency in yeast

Kyung Mi Choi; Young Yon Kwon; Cheol Koo Lee

doi:10.1016/j.febslet.2014.12.020

Disruption of Snf3/Rgt2 glucose sensors decreases lifespan and caloric restriction effectiveness through Mth1/Std1 by adjusting mitochondrial efficiency in yeast

Kyung Mi Choi, Young Yon Kwon, Cheol Koo Lee

Research output: Contribution to journal › Article › peer-review

11 Citations (Scopus)

Abstract

Down-regulation of intracellular nutrient signal pathways was proposed to be a primary mechanism of caloric restriction (CR)-mediated lifespan extension. However, the link between lifespan and glucose sensors in the plasma membrane was poorly understood in yeast. Herein, a mutant that lacked glucose sensors (snf3Δrgt2Δ) had impaired glucose fermentation, showed decreased chronological lifespan (CLS), and reduced CLS extension by CR. The mutant also had reduced mitochondrial efficiency, as inferred by increased mitochondrial superoxide and decreased ATP levels. Mth1 and Std1, which are downstream effectors of the Snf3/Rgt2 pathway, were required for viability through mitochondrial function but not fermentative metabolism.

Original language	English
Pages (from-to)	349-357
Number of pages	9
Journal	FEBS Letters
Volume	589
Issue number	3
DOIs	https://doi.org/10.1016/j.febslet.2014.12.020
Publication status	Published - 2015 Jan 30

Bibliographical note

Publisher Copyright:
© 2015 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.

Keywords

Chronological lifespan
Glucose sensor
Gpr1
Mitochondrial function
Rgt2
Snf3

ASJC Scopus subject areas

Biophysics
Structural Biology
Biochemistry
Molecular Biology
Genetics
Cell Biology

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10.1016/j.febslet.2014.12.020

Cite this

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title = "Disruption of Snf3/Rgt2 glucose sensors decreases lifespan and caloric restriction effectiveness through Mth1/Std1 by adjusting mitochondrial efficiency in yeast",

abstract = "Down-regulation of intracellular nutrient signal pathways was proposed to be a primary mechanism of caloric restriction (CR)-mediated lifespan extension. However, the link between lifespan and glucose sensors in the plasma membrane was poorly understood in yeast. Herein, a mutant that lacked glucose sensors (snf3Δrgt2Δ) had impaired glucose fermentation, showed decreased chronological lifespan (CLS), and reduced CLS extension by CR. The mutant also had reduced mitochondrial efficiency, as inferred by increased mitochondrial superoxide and decreased ATP levels. Mth1 and Std1, which are downstream effectors of the Snf3/Rgt2 pathway, were required for viability through mitochondrial function but not fermentative metabolism.",

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Disruption of Snf3/Rgt2 glucose sensors decreases lifespan and caloric restriction effectiveness through Mth1/Std1 by adjusting mitochondrial efficiency in yeast

Abstract

Bibliographical note

Keywords

ASJC Scopus subject areas

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