World Library  


Add to Book Shelf
Flag as Inappropriate
Email this Book

Plos Genetics : Deletion of the Mitochondrial Superoxide Dismutase Sod-2Extends Lifespan in Caenorhabditis Elegans, Volume 5

By Kim, Stuart K.

Click here to view

Book Id: WPLBN0003927682
Format Type: PDF eBook :
File Size:
Reproduction Date: 2015

Title: Plos Genetics : Deletion of the Mitochondrial Superoxide Dismutase Sod-2Extends Lifespan in Caenorhabditis Elegans, Volume 5  
Author: Kim, Stuart K.
Volume: Volume 5
Language: English
Subject: Journals, Science, Genetics
Collections: Periodicals: Journal and Magazine Collection (Contemporary), PLoS Genetics
Historic
Publication Date:
Publisher: Plos

Citation

APA MLA Chicago

Kim, S. K. (n.d.). Plos Genetics : Deletion of the Mitochondrial Superoxide Dismutase Sod-2Extends Lifespan in Caenorhabditis Elegans, Volume 5. Retrieved from http://www.ebooklibrary.org/


Description
Description : The oxidative stress theory of aging postulates that aging results from the accumulation of molecular damage caused by reactive oxygen species (ROS) generated during normal metabolism. Superoxide dismutases (SODs) counteract this process by detoxifying superoxide. It has previously been shown that elimination of either cytoplasmic or mitochondrial SOD in yeast, flies, and mice results in decreased lifespan. In this experiment, we examine the effect of eliminating each of the five individual sod genes present in Caenorhabditis elegans. In contrast to what is observed in other model organisms, none of the sod deletion mutants shows decreased lifespan compared to wild-type worms, despite a clear increase in sensitivity to paraquat- and juglone-induced oxidative stress. In fact, even mutants lacking combinations of two or three sod genes survive at least as long as wild-type worms. Examination of gene expression in these mutants reveals mild compensatory up-regulation of other sod genes. Interestingly, we find that sod-2 mutants are long-lived despite a significant increase in oxidatively damaged proteins. Testing the effect of sod-2 deletion on known pathways of lifespan extension reveals a clear interaction with genes that affect mitochondrial function : sod-2 deletion markedly increases lifespan in clk-1 worms while clearly decreasing the lifespan of isp-1 worms. Combined with the mitochondrial localization of SOD-2 and the fact that sod- 2 mutant worms exhibit phenotypes that are characteristic of long-lived mitochondrial mutants—including slow development, low brood size, and slow defecation—this suggests that deletion of sod-2 extends lifespan through a similar mechanism. This conclusion is supported by our demonstration of decreased oxygen consumption in sod-2 mutant worms. Overall, we show that increased oxidative stress caused by deletion of sod genes does not result in decreased lifespan in C. elegans and that deletion of sod-2 extends worm lifespan by altering mitochondrial function.

 

Click To View

Additional Books


  • Plos Genetics : the Abnormal Phenotypes ... (by )
  • Plos Genetics : Muscle-specific Splicing... (by )
  • Plos Genetics : Genetic Variants at Chro... (by )
  • Plos Genetics : Drosophila Melanogaster ... (by )
  • Plos Genetics : on the Analysis of Genom... (by )
  • Plos Genetics : Hierarchical Generalized... (by )
  • Plos Genetics : Deletion at Itpr1 Underl... (by )
  • Plos Genetics : Measures of Autozygosity... (by )
  • Plos Genetics : Pathogenic Vcp, Volume 7 (by )
  • Plos Genetics : Perspectives on Human Ge... (by )
  • Plos Genetics : Accurate Prediction of t... (by )
  • Plos Genetics : the Functional Interplay... (by )
Scroll Left
Scroll Right

 



Copyright © World Library Foundation. All rights reserved. eBooks from World eBook Library are sponsored by the World Library Foundation,
a 501c(4) Member's Support Non-Profit Organization, and is NOT affiliated with any governmental agency or department.