2024-03-28T17:13:51Zhttp://digital.csic.es/dspace-oai/requestoai:digital.csic.es:10261/425132021-12-27T15:40:56Zcom_10261_134com_10261_1col_10261_387
The Stress-activated Protein Kinase Hog1 Mediates S Phase Delay in Response to Osmostress
Yaakov, Gilad
Duch, Alba
García-Rubio, María L.
Clotet, Josep
Jiménez, Javier
Aguilera, Andrés
Posas, Francesc
Blotting
Cell cycle proteins
Immunoprecipitation
Osmotic pressure
Phosphorylation
Saccharomyces cerevisiae
DNA polymerase II
Cyclin B
11 páginas, 8 figuras.
Control of cell cycle progression by stress-activated protein kinases (SAPKs) is essential for cell adaptation to extracellular stimuli. Exposure of yeast to osmostress activates the Hog1 SAPK, which modulates cell cycle progression at G1 and G2 by the phosphorylation of elements of the cell cycle machinery, such as Sic1 and Hsl1, and by down-regulation of G1 and G2 cyclins. Here, we show that upon stress, Hog1 also modulates S phase progression. The control of S phase is independent of the S phase DNA damage checkpoint and of the previously characterized Hog1 cell cycle targets Sic1 and Hsl1. Hog1 uses at least two distinct mechanisms in its control over S phase progression. At early S phase, the SAPK prevents firing of replication origins by delaying the accumulation of the S phase cyclins Clb5 and Clb6. In addition, Hog1 prevents S phase progression when activated later in S phase or cells containing a genetic bypass for cyclin-dependent kinase activity. Hog1 interacts with components of the replication complex and delays phosphorylation of the Dpb2 subunit of the DNA polymerase. The two mechanisms of Hog1 action lead to delayed firing of origins and prolonged replication, respectively. The Hog1-dependent delay of replication could be important to allow Hog1 to induce gene expression before replication.
This work was supported by UNICELLSYS from the European Community's seventh framework program (FP7, agreement 201142) (to F. P.); the Spanish Ministry of Science and Innovation (grant BFU2006-00984) [to F. P.] and grant BFU2006-05260 [to A. A.)]; and Junta de Andalucía (CVI-624) (to A. A.) through contract ERAS-CT-2003-980409 of the European Commission, DG Research, FP6 as part of a EURYI scheme award (www.esf.org/euryi); and support from the Fundación Marcelino Botín (to F. P.) and Consolider Ingenio 2010 program (grant CSD2007-0015) of the Spanish Government (to F. P. and A. A.). F. P.'s research is supported by “ICREA Acadèmia” for excellence in research (Generalitat de Catalunya).
Peer reviewed
2011-11-16T18:00:30Z
2011-11-16T18:00:30Z
2009-05-28
artículo
http://purl.org/coar/resource_type/c_6501
Molecular Biology of the Cell 20(15): 3572-3582 (2009)
PMC2719575
PMID: 19477922
http://hdl.handle.net/10261/42513
10.1091/mbc.E09-02-0129
1939-4586
19477922
en
http://dx.doi.org/10.1091/mbc.E09-02-0129
open
American Society for Cell Biology