Can the different heat shock response thresholds found in fermenting and respiring yeast cells be attributed to their differential redox states?

Abstract

In this study we used a heat-shock (HS) reporter gene to demonstrate that respiring cells are intrinsically less sensitive (by 5 • C) than their fermenting counterparts to a sublethal heat shock. We also used an oxidant-sensitive fluorescent probe to demonstrate that this correlates with lower levels of sublethal reactive oxygen species (ROS) accumulation in heat-stressed respiring cells. Moreover, this relationship between HS induction of the reporter gene and ROS accumulation extends to respiring cells that have had their ROS levels modified by treatment with the antioxidant ascorbic acid and the pro-oxidant H 2 O 2 . Thus, by demonstrating that the ROS/HSR correlation previously demonstrated in fermenting cells also holds for respiring cells (despite their greater HS insensitivity and higher level of intrinsic thermotolerance), we provide evidence that the intracellular redox state may influence both the sensitivity of the heat-shock response (HSR) and stress tolerance in the yeast Saccharomyces cerevisiae.

Differential effects of hydrogen peroxide and ascorbic acid on the aerobic thermosensitivity of yeast cells grown under aerobic and anoxic conditions

“…In conclusion, the differential effects of H 2 O 2 and ascorbate on the aerobic thermosensitivity and intrinsic thermotolerance of yeast cells grown under different conditions reflect differences in the ever‐changing physiological dynamic and redox status of these cells. This study also reinforces our earlier work implicating the cellular redox potential as playing a key role in cellular thermosensitivity (Moraitis and Curran, 2004, 2007). Further investigations will reveal to what extent each of these factors contributes to such differential effects.…”

“…In accordance with a number of independent observations, we have previously shown that in aerobically‐grown yeast cells, the HSR is sensitized in the presence of H 2 O 2 and desensitized in the presence of ascorbate (Moraitis and Curran, 2004, 2007).…”

“…In agreement with the above, we have also demonstrated that in the yeast S. cerevisiae the inducibility of a HS‐reporter gene increases following H 2 O 2 pretreatment and decreases following ascorbate pretreatment, in both aerobically‐grown fermenting cells (Moraitis and Curran, 2004) and in respiring cells (Moraitis and Curran, 2007). These effects were differential between the two metabolic modes with respect to the concentration of H 2 O 2 required to increase cellular thermosensitivity and the extent of ascorbate's effect on decreasing cellular thermosensitivity.…”

“…These effects were differential between the two metabolic modes with respect to the concentration of H 2 O 2 required to increase cellular thermosensitivity and the extent of ascorbate's effect on decreasing cellular thermosensitivity. This reflects differences in the physiology and redox status between the two modes of growth (Moraitis and Curran, 2007). In this paper we examine the effect of exogenous H 2 O 2 and ascorbate on the aerobic thermosensitivity and intrinsic thermotolerance of yeast cells grown under anaerobic conditions, with two different lipid profiles.…”

An antioxidative mechanism mediated by the yeast N-acetyltransferase Mpr1: oxidative stress-induced arginine synthesis and its physiological role

“…Recently, we found that Mpr1 protects yeast cells by reducing the intracellular reactive oxygen species (ROS) levels under oxidative stress conditions, such as H 2 O 2 , heat shock, freeze–thaw or ethanol treatment (Nomura & Takagi, 2004; Du & Takagi, 2005, 2007). Exposure to a high temperature also produces ROS in the mitochondria, which cause oxidative stress in yeast cells (Davidson et al , 1996; Moraitis & Curran, 2004, 2007). We also isolated two Mpr1 variants with improved enzymatic functions (K63R and F65L) (Iinoya et al , 2009).…”