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Bax inhibitor-1 (BI-1) is an evolutionarily conserved cell death suppresser in animals, yeast, and plants. In this study, yeast strains carrying single-gene deletions were screened for factors related to cell death suppression by Arabidopsis BI-1 (AtBI-1). Our screen identified mutants that failed to survive Bax-induced lethality even with AtBI-1 coexpression (Bax suppressor). The Dcox16 strain was isolated as a BI-1-inactive mutant; it was disrupted in a component of the mitochondrial cytochrome c oxidase. Other mutants defective in mitochondrial electron transport showed a similar phenotype. ATP levels were markedly decreased in all these mutants, suggesting that BI-1 requires normal electron transport activity to suppress cell death in yeast.

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Manganese (Mn) accumulates at a higher level in the pancreas than in any other organs when excess Mn is administered to the rat. The present study is carded out to analyze the intracellular localization of Mn existed in the pancreatic cell of Mn‐treated rats. Transmission electron microscope and X‐ray micro‐analysis connected with a rapid freezing fixation technique showed that a large amount of Mn was localized in tysosomal particles of the pancreatic cell of Mn‐treated rats. The Mn‐rich particles disappeared when the element‐administration was discontinued, showing that the accumulation of Mn is reversible. To confirm that Mn is in the lysosomes, a centrifugal subcellular‐fractionation and a neutron activation analysis were carried out. The result indicated that much Mn existed in the lysosomal fraction.