Abstract
Industrial production of bioethanol from lignocellulosic materials (LCM′s) is reliant on a microorganism being tolerant to the stresses inherent to fermentation. Previous work has highlighted the importance of a cytochrome oxidase chaperone gene (COX20) in improving yeast tolerance to acetic acid, a common inhibitory compound produced during pre-treatment of LCM’s. The presence of acetic acid has been shown to induce oxidative stress and programmed cell death, so the role of COX20 in oxidative stress was determined. Analysis using flow cytometry revealed that COX20 expression was associated with reduced levels of reactive oxygen species (ROS) in hydrogen peroxide and metal-induced stress, and there was a reduction in apoptotic and necrotic cells when compared with a strain without COX20. Results on the functionality of COX20 have revealed that overexpression of COX20 induced respiratory growth in Δimp1 and Δcox18, two genes whose presence is essential for yeast respiratory growth. COX20 also has a role in protecting the yeast cell against programmed cell death.
Highlights
During fermentation, yeast is exposed to a range of cellular stresses such as accumulation of toxic end products such as ethanol or butanol, a shift into more acidic pH, anaerobic growth conditions and nutrient limitation [1]
Previous work has shown that COX20 is upregulated in the presence of acetic acid, and its overexpression protects the cell against hydrogen peroxide-induced oxidative stress [15]
Assays with 0.5 M pyocyanin (0.5 M was chosen as this concentration has been shown to induce oxidative stress in S. cerevisiae BY4741 [16]), revealed that 22.92 ± 0.25% of BY4741 cells were redox stressed, deletion of cox20 increased the presence of redox stressed yeast cells to 37.5 ± 0.35%; overexpression of COX20 reduced the number of redox stressed cells to 16.09 ± 0.48% (Figure 1D–F)
Summary
Yeast is exposed to a range of cellular stresses such as accumulation of toxic end products such as ethanol or butanol, a shift into more acidic pH, anaerobic growth conditions and nutrient limitation [1]. The presence of ROS can disrupt a diverse array of biological processes [5] and has been shown to damage a variety of cellular components, including DNA, proteins, and unsaturated lipids [6]. Yeasts’ response to the presence of ROS is diverse, with an enzymatic response, such as the upregulation of thioredoxins, glutaredoxins, catalases, superoxide dismutase, and a non-enzymatic cellular response (such as glutathione becoming oxidized and being recycled) [10,11,12]. Previous work has shown that COX20 is upregulated in the presence of acetic acid, and its overexpression protects the cell against hydrogen peroxide-induced oxidative stress [15]. Programmed cell death in yeast can be induced by the addition of acetic acid, whose presence can induce a cytochrome c cascade from the mitochondria
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