ArticleMicrobial cell (Graz, Austria)2015
The MAPKKKs Ste11 and Bck1 jointly transduce the high oxidative stress signal through the cell wall integrity MAP kinase pathway.
Article in Microbial cell (Graz, Austria), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 20 citations in OpenAlex.
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- Advances in Protein Kinase Regulation of Stress Responses in Fruits and Vegetables.International journal of molecular sciences · 2025Review
- The Viral K1 Killer Yeast System: Toxicity, Immunity, and Resistance.Yeast (Chichester, England) · 2024Review
- Cdk8 Kinase Module: A Mediator of Life and Death Decisions in Times of Stress.Microorganisms · 2021Review
- Reprogramming of the Ethanol Stress Response in Saccharomyces cerevisiae by the Transcription Factor Znf1 and Its Effect on the Biosynthesis of Glycerol and Ethanol.Applied and environmental microbiology · 2021Article
- Article
- TheeLife · 2020Article
- Ubiquitin-proteasome-mediated cyclin C degradation promotes cell survival following nitrogen starvation.Molecular biology of the cell · 2020Article
- CgSTE11 mediates cross tolerance to multiple environmental stressors in Candida glabrata.Scientific reports · 2019Article
- Cyclin C: The Story of a Non-Cycling Cyclin.Biology · 2019Review
- A complex molecular switch directs stress-induced cyclin C nuclear release through SCFMolecular biology of the cell · 2018Article
- Feelin' it: Differential oxidative stress sensing mediated by Cyclin C.Microbial cell (Graz, Austria) · 2015Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Oxidative stress stimulates the Rho1 GTPase, which in turn induces the cell wall integrity (CWI) MAP kinase cascade. CWI activation promotes stress-responsive gene expression through activation of transcription factors (Rlm1, SBF) and nuclear release and subsequent destruction of the repressor cyclin C. This study reports that, in response to high hydrogen peroxide exposure, or in the presence of constitutively active Rho1, cyclin C still translocates to the cytoplasm and is degraded in cells lacking Bck1, the MAPKKK of the CWI pathway. However, in mutants defective for both Bck1 and Ste11, the MAPKKK from the high osmolarity, pseudohyphal and mating MAPK pathways, cyclin C nuclear to cytoplasmic relocalization and destruction is prevented. Further analysis revealed that cyclin C goes from a diffuse nuclear signal to a terminal nucleolar localization in this double mutant. Live cell imaging confirmed that cyclin C transiently passes through the nucleolus prior to cytoplasmic entry in wild-type cells. Taken together with previous studies, these results indicate that under low levels of oxidative stress, Bck1 activation is sufficient to induce cyclin C translocation and degradation. However, higher stress conditions also stimulate Ste11, which reinforces the stress signal to cyclin C and other transcription factors. This model would provide a mechanism by which different stress levels can be sensed and interpreted by the cell.
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