2004
DOI: 10.1099/mic.0.27162-0
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Stress induces depletion of Cdc25p and decreases the cAMP producing capability in Saccharomyces cerevisiae

Abstract: In Saccharomyces cerevisiae the cAMP-dependent protein kinase A pathway antagonizes the cellular response to stress. It is shown here that the cellular content of Cdc25p, the upstream activator of Ras and adenylyl cyclase, decays upon various stresses such as heat shock and oxidative and ethanol shocks, whereas its phosphorylation level and its localization are unaffected. In parallel with the reduction of Cdc25p, the maximal capacity of the cell to accumulate cAMP decreases when its feedback regulation is abo… Show more

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Cited by 26 publications
(18 citation statements)
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“…Like Hsf1, Msn2/4 is hyperphosphorylated in response to heat shock, but this modification is inhibited by cAMP, suggesting that it is not mediated by PKA (Garreau et al 2000). Heat shock, oxidative and ethanol stress moderately reduce cAMP levels via destabilization of the Ras activator, Cdc25, leading to speculation that cAMP/PKA may yet be the nexus of ESR signaling and that additional phosphorylation events may act as subordinate modulators of the response (Wang et al 2004). Activation of the cell wall integrity pathway by heat shock has been reviewed elsewhere, but importantly is insulated from Hsf1 or Msn2/4 activation and is not affected by cAMP/PKA (Levin 2005).…”
Section: Control and Regulation Of The Heat Shock Responsementioning
confidence: 99%
“…Like Hsf1, Msn2/4 is hyperphosphorylated in response to heat shock, but this modification is inhibited by cAMP, suggesting that it is not mediated by PKA (Garreau et al 2000). Heat shock, oxidative and ethanol stress moderately reduce cAMP levels via destabilization of the Ras activator, Cdc25, leading to speculation that cAMP/PKA may yet be the nexus of ESR signaling and that additional phosphorylation events may act as subordinate modulators of the response (Wang et al 2004). Activation of the cell wall integrity pathway by heat shock has been reviewed elsewhere, but importantly is insulated from Hsf1 or Msn2/4 activation and is not affected by cAMP/PKA (Levin 2005).…”
Section: Control and Regulation Of The Heat Shock Responsementioning
confidence: 99%
“…Although the NLS is controlled by four phosphorylation sites (Gorner et al 1998), we considered only one phosphorylation-dephosphorylation event in our simplified model because this is sufficient to couple the shuttling of Msn2 to the oscillatory dynamics of the cAMP-PKA system. The effect of stress is likely manifold: regardless of its precise nature-be it chemical, light emitted from the microscope, or carbon source limitation-we assumed that it controls the cAMP-PKA pathway through the inactivation of GEF (Wang et al 2004), and enhances the activity of phosphatases acting on Msn2, as can be deduced from the experimental results showing that Msn2 still responds to stress by entering the nucleus in the absence of any variation in cAMP (Garmendia-Torres et al 2007). …”
Section: Presentation Of the Deterministic Modelmentioning
confidence: 99%
“…It is known that sexual development of Volvox is not only induced by the sex-inducer but also in response to heat and oxidative stress (Kirk and Kirk 1986;Nedelcu 2005;Nedelcu and Michod 2003) and also light plays a critical role in the success of this sexual induction (Starr et al 1980). In this regard, it is remarkable that cAMP has been shown to be involved in responses to heat and oxidative stress (Taminato et al 2002;Wang et al 2004). Provided that histidine kinase rhodopsins of V. carteri with adenyl cyclase activity can produce cAMP in a light-dependent manner in response to environmental signal inputs, it is likely that they participate in sexual development (Fig.…”
Section: Histidine Kinase Rhodopsinsmentioning
confidence: 99%