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The crucial role of mitochondrial regulation in adaptive aluminium resistance in Rhodotorula glutinis

Authors :
Tani, Akio
Inoue, Chiemi
Tanaka, Yoko
Yamamoto, Yoko
Kondo, Hideki
Hiradate, Syuntaro
Kimbara, Kazuhide
Kawai, Fusako
Source :
Microbiology. Nov, 2008, Vol. 154 Issue 11, p3437, 10 p.
Publication Year :
2008

Abstract

Rhodotorula glutinis IFO1125 was found to acquire increased aluminium (AI) resistance from 50 [micro]M to more than 5 mM by repetitive culturing with stepwise increases in AI concentration at pH 4.0. To investigate the mechanism underlying this novel phenomenon, wild-type and AI-resistant cells were compared. Neither cell type accumulated the free form of AI ([AI.sup.3+]) added to the medium. Transmission electron microscopic analyses revealed a greater number of mitochondria in resistant cells. The formation of small mitochondria with simplified cristae structures was observed in the wild-type strain grown in the presence of AI and in resistant cells grown in the absence of AI. Addition of AI to cells resulted in high mitochondrial membrane potential and concomitant generation of reactive oxygen species (ROS). Exposure to AI also resulted in elevated levels of oxidized proteins and oxidized lipids. Addition of the antioxidants [alpha]-tocopherol and ascorbic acid alleviated the AI toxicity, suggesting that ROS generation is the main cause of AI toxicity. Differential display analysis indicated upregulation of mitochondrial genes in the resistant cells. Resistant cells were found to have 2.5- to 3-fold more mitochondrial DNA (mtDNA) than the wild-type strain. Analysis of tricarboxylic acid cycle and respiratory-chain enzyme activities in wild-type and resistant cells revealed significantly reduced cytochrome c oxidase activity and resultant high ROS production in the latter cells. Taken together, these data suggest that the adaptive increased resistance to AI stress in resistant cells resulted from an increased number of mitochondria and increased mtDNA content, as a compensatory response to reduced respiratory activity caused by a deficiency in complex IV function.

Details

Language :
English
ISSN :
13500872
Volume :
154
Issue :
11
Database :
Gale General OneFile
Journal :
Microbiology
Publication Type :
Academic Journal
Accession number :
edsgcl.190099402