Document Detail


Metabolome analysis of response to oxidative stress in rice suspension cells overexpressing cell death suppressor Bax inhibitor-1.
MedLine Citation:
PMID:  19919949     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Bax inhibitor-1 (BI-1) is a cell death suppression factor widely conserved in higher plants and animals. Overexpression of Arabidopsis BI-1 (AtBI-1) in plants confers tolerance to various cell death-inducible stresses. However, apart from the cell death-suppressing activity, little is known about the physiological roles of BI-1-overexpressing plants. In this study, we evaluated the effects of AtBI-1 overexpression on the rice metabolome in response to oxidative stress. AtBI-1-overexpressing rice cells in suspension displayed enhanced tolerance to menadione-induced oxidative stress compared with vector control cells, whereas AtBI-1 overexpression did not influence the increase of intracellular H(2)O(2) concentration or inhibition of oxidative stress-sensitive aconitase activity. Capillary electrophoresis-mass spectrometry (CE-MS)-based metabolome analysis revealed dynamic metabolic changes in oxidatively stressed rice cells, e.g. depletion of the central metabolic pathway, imbalance of the redox state and energy charge, and accumulation of amino acids. Furthermore, comparative metabolome analysis demonstrated that AtBI-1 overexpression did not affect primary metabolism in rice cells under normal growth conditions but significantly altered metabolite composition within several distinct pathways under cell death-inducible oxidative stress. The AtBI-1-mediated metabolic alteration included recovery of the redox state and energy charge, which are known as important factors for metabolic defense against oxidative stress. These observations suggest that although AtBI-1 does not affect rice metabolism directly, its cell death suppression activity leads to enhanced capacity to acclimate oxidative stress.
Authors:
Toshiki Ishikawa; Kentaro Takahara; Takayuki Hirabayashi; Hideo Matsumura; Shizuko Fujisawa; Ryohei Terauchi; Hirofumi Uchimiya; Maki Kawai-Yamada
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2009-11-16
Journal Detail:
Title:  Plant & cell physiology     Volume:  51     ISSN:  1471-9053     ISO Abbreviation:  Plant Cell Physiol.     Publication Date:  2010 Jan 
Date Detail:
Created Date:  2010-01-18     Completed Date:  2010-04-16     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9430925     Medline TA:  Plant Cell Physiol     Country:  Japan    
Other Details:
Languages:  eng     Pagination:  9-20     Citation Subset:  IM    
Affiliation:
Graduate School of Science and Engineering, Saitama University, Saitama, Japan.
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MeSH Terms
Descriptor/Qualifier:
Adaptation, Physiological / genetics
Amino Acids / metabolism
Apoptosis Regulatory Proteins / genetics*,  metabolism*
Arabidopsis Proteins / genetics,  metabolism
Cell Death / genetics
Drug Resistance / genetics
Electrophoresis, Capillary
Energy Metabolism / genetics
Gene Expression Regulation, Plant / physiology
Mass Spectrometry
Membrane Proteins / genetics,  metabolism
Metabolome / genetics*
Oryza sativa / cytology,  genetics*,  metabolism*
Oxidation-Reduction
Oxidative Stress / genetics*
Plant Proteins / genetics,  metabolism
Vitamin K 3 / toxicity
Vitamins / toxicity
Chemical
Reg. No./Substance:
0/ATBI-1 protein, Arabidopsis; 0/Amino Acids; 0/Apoptosis Regulatory Proteins; 0/Arabidopsis Proteins; 0/Membrane Proteins; 0/Plant Proteins; 0/Vitamins; 58-27-5/Vitamin K 3

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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