Induction of increased thermotolerance in Saccharomyces cerevisiae may be triggered by a mechanism involving intracellular pH

Coote, Peter J.; Cole, M.; Jones, Martin V.

doi:10.1099/00221287-137-7-1701

Cited by 100 publications

(79 citation statements)

References 42 publications

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“…It is difficult to assess this study as the conditions, notably pH, of growth were not reported. Coote et al (1991) showed thermotolerance increasing during a 9 mM sorbic acid treatment, both at pH 4.5 and at pH 6.0. However, a partial thermotolerance increase was also seen in cells exposed to pH 4-5 in the absence of sorbate.…”

Section: The Effects Of Sorbate On Thermotolerancementioning

confidence: 99%

Weak acid preservatives block the heat shock response and heat-shock-element-directed lacZ expression of low pH Saccharomyces cerevisiae cultures, an inhibitory action partially relieved by respiratory deficiency

Cheng

Piper

1994

Microbiology

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Inhibition of microbial growth by weak acid preservatives increases with medium acidification, since these agents enter cells in the undissociated state. Many of the effects of these acids are due to the cytoplasmic acidification they cause as they dissociate in the higher pH environment of the cytosol. Sorbic and benzoic acids, two widely used preservatives, were found to exert pronounced effects on the heat shock response and thermotolerance of Saccharomyces cerevisiae. These effects were strongly influenced by the pH of the culture medium. In low pH cultures sorbate inhibited the induction of thermotolerance by sublethal heat shock, causing strong induction of respiratory-deficient petites among the survivors of heat treatment. However, when the culture pH was above 5-5 sorbate acted as a powerful chemical inducer of thermotolerance in the absence of any sublethal heat treatment. Sorbate and benzoate also inhibited heat induction of the major heat shock proteins in low pH yeast cultures. This appears to result from lack of induction of the heat shock element (HSE) promoter sequence since sorbate prevented heat induction of a HSE-lacZ fusion a t low pH. The uncoupler carbonyl cyanide m-chlorophenylhydrazone (CCCP) and the plasma-membrane-ATPase inhibitor diethylstilboestrol were identified as additional inhibitors of heat induction of heat shock proteins. Numerous chemicals induce the heat shock response in the absence of heat stress, but sorbate, benzoate, CCCP and diethylstilboestrol are the first compounds shown to act as selective inhibitors of heat-induced protein expression in yeast. In the presence of sorbate concentrations which, a t low pH, totally inhibit both the heat shock response and growth of cells competent in respiration, respiratory-def icient petites still retain a limited capacity for growth and for heat induction of heat shock proteins. This restoration of a response to heat shock in acidified sorbate-treated cultures of petites might contribute to their higher capacity for growth in the presence of sorbate.

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Section: The Effects Of Sorbate On Thermotolerancementioning

confidence: 99%

Weak acid preservatives block the heat shock response and heat-shock-element-directed lacZ expression of low pH Saccharomyces cerevisiae cultures, an inhibitory action partially relieved by respiratory deficiency

Cheng

Piper

1994

Microbiology

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“…These include an increase in membrane permeability and passive proton influx, and a dissipation of the proton motive force across the plasma membrane. The level of the plasma membrane H + -ATPase declines following exposure to ethanol or heat, but the activity of the residual enzyme increases dramatically (Coote et al, 1991(Coote et al, , 1994Rosa and Sá-Correia, 1991;Monteiro and Sá-Correia, 1998;Piper et al, 1994). Consequently, more ATP is spent by the cells in response to ethanol stress or heat shock.…”

Section: Introductionmentioning

confidence: 99%

Endocytosis and vacuolar morphology inSaccharomyces cerevisiae are altered in response to ethanol stress or heat shock

Meaden¹,

Arneborg²,

Guldfeldt³

et al. 1999

Yeast

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“…Adapted cells are not only able to resume growth, but are also more protected when exposed to a new stress situation (Trollmo et al, 1988;Varela et al, 1992). This protection is not only limited to a second challenge of the same kind of stress, but also to other types of stress, indicating that the stress response consists of both specific and general elements (Coote et al, 1991;Trollmo et al, 1988;Varela et al, 1992).…”

Section: Introductionmentioning

confidence: 99%

High-osmolarity signalling in Saccharomyces cerevisiae is modulated in a carbon-source-dependent fashion

Siderius¹,

Rots²,

Mager³

1997

Microbiology

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High-osmolarity-induced expression of the small heat-shock gene HSP12 is regulated by the HOG (high-osmolarity glycerol) pathway and PKA (protein kinase A). To analyse the regulatory input of both signal transduction pathways, high-salt-induced HSP12 expression in different genetic backgrounds on glucose-, ethanol- and glycerol-based culture media was examined. Upon exposure to high-osmolarity stress, the kinetics of induction of HSP12 in cells growing on the non-fermentable carbon sources are strikingly different from those on glucose. Derepression of HSP12 gene expression under non-stress conditions was observed in cells growing on non-fermentable carbon sources. High-salt challenge resulted in a lower induction of the HSP12 mRNA levels in ethanol-grown cells as compared to glucose-grown cells, whereas in glycerol-grown cells hardly any high-salt induction of HSP12 mRNA levels could be detected. Analysis of signalling through the HOG pathway suggested that glycerol may influence the activity of this signalling route, possibly via negative feedback. Furthermore, the cellular level of PKA activity was found to have a great impact on stress-responsive gene transcription. On the basis of the data obtained it was concluded that modulation of PKA activity plays a major role in the stress response. A glucose-dependent, PKA-regulated cellular component is postulated to affect high-osmolarity-induced HSP12 expression.

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Induction of increased thermotolerance in Saccharomyces cerevisiae may be triggered by a mechanism involving intracellular pH

Cited by 100 publications

References 42 publications

Weak acid preservatives block the heat shock response and heat-shock-element-directed lacZ expression of low pH Saccharomyces cerevisiae cultures, an inhibitory action partially relieved by respiratory deficiency

Weak acid preservatives block the heat shock response and heat-shock-element-directed lacZ expression of low pH Saccharomyces cerevisiae cultures, an inhibitory action partially relieved by respiratory deficiency

Endocytosis and vacuolar morphology inSaccharomyces cerevisiae are altered in response to ethanol stress or heat shock

High-osmolarity signalling in Saccharomyces cerevisiae is modulated in a carbon-source-dependent fashion

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