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Sci. Signal., 27 September 2011
Vol. 4, Issue 192, p. ra63
[DOI: 10.1126/scisignal.2002204]


Editor's Summary

Assigning Roles to the Arrest Team
To avoid replicating under suboptimal conditions, cells have elaborate mechanisms to sense and respond to stressful conditions and halt progression through the cell cycle. In budding yeast, the stress-activated protein kinase Hog1 prevents progression through the cell cycle by arresting the cells in the G1 phase when yeast are exposed to hyperosmotic stress. Using a combination of in vivo experiments, modeling, and simulation, Adrover et al. quantitatively investigated the temporal dynamics of this cell cycle arrest. They defined the specific roles of components downstream of Hog1 in preventing the G1-to-S phase transition and budding in response to hyperosmotic stress. Their analyses suggested that Hog1-mediated inhibition of the expression of the gene encoding the S-phase cyclin Clb5 was a key determinant of osmotic stress–induced G1 arrest.

Citation: M. A. Adrover, Z. Zi, A. Duch, J. Schaber, A. González-Novo, J. Jimenez, M. Nadal-Ribelles, J. Clotet, E. Klipp, F. Posas, Time-Dependent Quantitative Multicomponent Control of the G1-S Network by the Stress-Activated Protein Kinase Hog1 upon Osmostress. Sci. Signal. 4, ra63 (2011).

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Response to Hyperosmotic Stress.
H. Saito and F. Posas (2012)
Genetics 192, 289-318
   Abstract »    Full Text »    PDF »
The p57 CDKi integrates stress signals into cell-cycle progression to promote cell survival upon stress.
M. Joaquin, A. Gubern, D. Gonzalez-Nunez, E. Josue Ruiz, I. Ferreiro, E. de Nadal, A. R. Nebreda, and F. Posas (2012)
EMBO J. 31, 2952-2964
   Abstract »    Full Text »    PDF »

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