Caloric restriction restores the chronological life span of the goa1 null mutant of Candida albicans in spite of high cell levels of ROS

2012 ◽  
Vol 49 (12) ◽  
pp. 1023-1032 ◽  
Author(s):  
Hui Chen ◽  
Richard Calderone ◽  
Nuo Sun ◽  
Yun Wang ◽  
Dongmei Li
2012 ◽  
Vol 16 (1) ◽  
pp. 55-67 ◽  
Author(s):  
Alejandro Ocampo ◽  
Jingjing Liu ◽  
Elizabeth A. Schroeder ◽  
Gerald S. Shadel ◽  
Antoni Barrientos

2017 ◽  
Vol 37 (13) ◽  
Author(s):  
Margaret B. Wierman ◽  
Nazif Maqani ◽  
Erika Strickler ◽  
Mingguang Li ◽  
Jeffrey S. Smith

ABSTRACT AMP-activated protein kinase (AMPK) and the homologous yeast SNF1 complex are key regulators of energy metabolism that counteract nutrient deficiency and ATP depletion by phosphorylating multiple enzymes and transcription factors that maintain energetic homeostasis. AMPK/SNF1 also promotes longevity in several model organisms, including yeast. Here we investigate the role of yeast SNF1 in mediating the extension of chronological life span (CLS) by caloric restriction (CR). We find that SNF1 activity is required throughout the transition of log phase to stationary phase (diauxic shift) for effective CLS extension. CR expands the period of maximal SNF1 activation beyond the diauxic shift, as indicated by Sak1-dependent T210 phosphorylation of the Snf1 catalytic α-subunit. A concomitant increase in ADP is consistent with SNF1 activation by ADP in vivo. Downstream of SNF1, the Cat8 and Adr1 transcription factors are required for full CR-induced CLS extension, implicating an alternative carbon source utilization for acetyl coenzyme A (acetyl-CoA) production and gluconeogenesis. Indeed, CR increased acetyl-CoA levels during the diauxic shift, along with expression of both acetyl-CoA synthetase genes ACS1 and ACS2. We conclude that CR maximizes Snf1 activity throughout and beyond the diauxic shift, thus optimizing the coordination of nucleocytosolic acetyl-CoA production with massive reorganization of the transcriptome and respiratory metabolism.


Genetics ◽  
2003 ◽  
Vol 163 (1) ◽  
pp. 35-46 ◽  
Author(s):  
Paola Fabrizio ◽  
Lee-Loung Liou ◽  
Vanessa N Moy ◽  
Alberto Diaspro ◽  
Joan Selverstone Valentine ◽  
...  

Abstract Signal transduction pathways inactivated during periods of starvation are implicated in the regulation of longevity in organisms ranging from yeast to mammals, but the mechanisms responsible for life-span extension are poorly understood. Chronological life-span extension in S. cerevisiae cyr1 and sch9 mutants is mediated by the stress-resistance proteins Msn2/Msn4 and Rim15. Here we show that mitochondrial superoxide dismutase (Sod2) is required for survival extension in yeast. Deletion of SOD2 abolishes life-span extension in sch9Δ mutants and decreases survival in cyr1:mTn mutants. The overexpression of Sods—mitochondrial Sod2 and cytosolic CuZnSod (Sod1)—delays the age-dependent reversible inactivation of mitochondrial aconitase, a superoxide-sensitive enzyme, and extends survival by 30%. Deletion of the RAS2 gene, which functions upstream of CYR1, also doubles the mean life span by a mechanism that requires Msn2/4 and Sod2. These findings link mutations that extend chronological life span in S. cerevisiae to superoxide dismutases and suggest that the induction of other stress-resistance genes regulated by Msn2/4 and Rim15 is required for maximum longevity extension.


2017 ◽  
Vol 292 (2) ◽  
pp. 475-481 ◽  
Author(s):  
Takafumi Shimasaki ◽  
Hokuto Ohtsuka ◽  
Chikako Naito ◽  
Kenko Azuma ◽  
Takeshi Tenno ◽  
...  

2019 ◽  
Vol 366 (8) ◽  
Author(s):  
Subasri Subramaniyan ◽  
Phaniendra Alugoju ◽  
Sudharshan SJ ◽  
Bhavana Veerabhadrappa ◽  
Madhu Dyavaiah

1995 ◽  
Vol 217 (2) ◽  
pp. 309-316 ◽  
Author(s):  
William R. Pendergrass ◽  
Yi Li ◽  
DeZhao Jiang ◽  
R.G. Fei ◽  
Norman S. Wolf

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