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

Fusako Kawai^1,

¹ Research Institute for Bioresources, Okayama University, 2-20-1 Chuo, Kurashiki, Okayama 710-0046, Japan
² National Institute for Agro-Environmental Sciences, 3-1-3 Kan-nondai, Tsukuba, Ibaragi 305-8604, Japan

Correspondence
Fusako Kawai
fkawai{at}kit.ac.jp

Rhodotorula glutinis IFO1125 was found to acquire increased aluminium (Al) resistance from 50 µM to more than 5 mM by repetitive culturing with stepwise increases in Al concentration at pH 4.0. To investigate the mechanism underlying this novel phenomenon, wild-type and Al-resistant cells were compared. Neither cell type accumulated the free form of Al (Al³⁺) 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 Al and in resistant cells grown in the absence of Al. Addition of Al to cells resulted in high mitochondrial membrane potential and concomitant generation of reactive oxygen species (ROS). Exposure to Al also resulted in elevated levels of oxidized proteins and oxidized lipids. Addition of the antioxidants -tocopherol and ascorbic acid alleviated the Al toxicity, suggesting that ROS generation is the main cause of Al 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 Al 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.

Present address: R&D; Center for Bio-based Materials, Kyoto Institute of Technology, Matsugasaki, Sakyo-ku, Kyoto 606-8585, Japan (fkawai{at}kit.ac.jp).

The GenBank/EMBL/DDBJ accession numbers for the DNA sequences reported in this paper are AB248915 (partial mtDNA) and AB248916 (partial actin gene).