Research Article: Peroxisomal catalase deficiency modulates yeast lifespan depending on growth conditions

Date Published: January 19, 2013

Publisher: Impact Journals LLC

Author(s): Adam Kawałek, Sophie D. Lefevre, Marten Veenhuis, Ida J. van der Klei.

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Abstract

We studied the role of peroxisomal catalase in chronological aging of the yeastHansenula polymorpha in relation to various growth substrates. Catalase-deficient (cat) cells showed a similar chronological life span (CLS) relative to the wild-type control upon growth on carbon and nitrogen sources that are not oxidized by peroxisomal enzymes. However, when media contained methylamine, which is oxidized by peroxisomal amine oxidase, the CLS of cat cells was significantly reduced. Conversely, the CLS of cat cells was enhanced relative to the wild-type control, when cells were grown on methanol, which is oxidized by peroxisomal alcohol oxidase. At these conditions strongly enhanced ROS levels were observed during the exponential growth phase of cat cells. This was paralleled by activation of the transcription factor Yap1, as well as an increase in the levels of the antioxidant enzymes cytochrome c peroxidase and superoxide dismutase. Upon deletion of the genes encoding Yap1 or cytochrome c peroxidase, the CLS extension of cat cells on methanol was abolished. These findings reveal for the first time an important role of enhanced cytochrome c peroxidase levels in yeast CLS extension.

Partial Text

Aging is defined as progressive deterioration of cellular components resulting in loss of function and cell death. Reactive oxygen species (ROS) are considered to play a pivotal role in this process. Until recently ROS were assumed to represent toxic by-products of cellular metabolism, which inflict damage to important macromolecules such as DNA, lipids and proteins [1, 2]. Indeed, when cells age oxidative stress increases paralleled by the accumulation of oxidatively damaged macromolecules. However, recent findings indicate that this cannot fully explain age associated functional losses. Instead, ROS were shown to be crucial in several important cellular processes such as signal transduction, gene regulation, and redox regulation [3-5]. As a consequence, their complete elimination would be harmful to cells. These observations resulted in an alternative hypothesis, designated “the redox stress hypothesis”, which proposes that age-associated functional losses are caused by progressive oxidation of redox-sensitive protein thiols and consequent disruption of the redox-regulated signaling mechanisms [6].

In yeast two types of aging have been defined, namely chronological and replicative aging. The chronological lifespan is the time cells can survive in a non-dividing state, whereas the replicative lifespan represent the number of buds a mother cell produces before it dies. These two types of aging are regulated by partially overlapping regulatory mechanisms. Several recent studies focused on the role of acidification, which accelerates both modes of aging in yeast as well as in mammalian cells [38,39]. Here we studied the role of another important factor in aging, namely reactive oxygen species (ROS).

 

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