ArticleMolecular biology of the cell2007
Regulation of cell cycle and stress responses to hydrostatic pressure in fission yeast.
Article in Molecular biology of the cell, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
10 citing papers in PubMed, 25 citations in OpenAlex.
- The genome of an apodid holothuroid (Chiridota heheva) provides insights into its adaptation to a deep-sea reducing environment.Communications biology · 2022Article
- Article
- The Fission Yeast Cell Integrity Pathway: A Functional Hub for Cell Survival upon Stress and Beyond.Journal of fungi (Basel, Switzerland) · 2021Review
- Inactive Tlk associating with Tak1 increases p38 MAPK activity to prolong the G2 phase.Scientific reports · 2019Article
- A novel live-cell imaging system reveals a reversible hydrostatic pressure impact on cell-cycle progression.Journal of cell science · 2018Article
- Article
- The centrosome and its duplication cycle.Cold Spring Harbor perspectives in biology · 2015Review
- Nutrient limitations alter cell division control and chromosome segregation through growth-related kinases and phosphatases.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2011Review
- Biotechnological properties of distillery and laboratory yeasts in response to industrial stresses.Journal of industrial microbiology & biotechnology · 2010Article
- Stress signalling to fungal stress-activated protein kinase pathways.FEMS microbiology letters · 2010Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
We have investigated the cellular responses to hydrostatic pressure by using the fission yeast Schizosaccharomyces pombe as a model system. Exposure to sublethal levels of hydrostatic pressure resulted in G2 cell cycle delay. This delay resulted from Cdc2 tyrosine-15 (Y-15) phosphorylation, and it was abrogated by simultaneous disruption of the Cdc2 kinase regulators Cdc25 and Wee1. However, cell cycle delay was independent of the DNA damage, cytokinesis, and cell size checkpoints, suggesting a novel mechanism of Cdc2-Y15 phosphorylation in response to hydrostatic pressure. Spc1/Sty1 mitogen-activated protein (MAP) kinase, a conserved member of the eukaryotic stress-activated p38, mitogen-activated protein (MAP) kinase family, was rapidly activated after pressure stress, and it was required for cell cycle recovery under these conditions, in part through promoting polo kinase (Plo1) phosphorylation on serine 402. Moreover, the Spc1 MAP kinase pathway played a key role in maintaining cell viability under hydrostatic pressure stress through the bZip transcription factor, Atf1. Further analysis revealed that prestressing cells with heat increased barotolerance, suggesting adaptational cross-talk between these stress responses. These findings provide new insight into eukaryotic homeostasis after exposure to pressure stress.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.