Evidence map›Paper›PMID 19477922›Full record

ArticleMolecular biology of the cell2009

The stress-activated protein kinase Hog1 mediates S phase delay in response to osmostress.

Gilad Yaakov, Alba Duch, María García-Rubio, Josep Clotet, Javier Jimenez, Andrés Aguilera, Francesc Posas

Open access · greenAbstract read
In one paragraph

Article in Molecular biology of the cell, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
3.1field-weighted citation impact, top 8% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

33 citing papers in PubMed, 64 citations in OpenAlex.

  1. HOG Signaling: A Multifunctional Regulator of Stress Homeostasis inJournal of fungi (Basel, Switzerland) · 2026
    Review
  2. Review
  3. Article
  4. Dynamic phosphorylation of Hcm1 promotes fitness in chronic stress.bioRxiv : the preprint server for biology · 2025
    Article
  5. Article
  6. Advances inJournal of fungi (Basel, Switzerland) · 2023
    Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Hog1 activation delays mitotic exit via phosphorylation of Net1.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Stress Adaptation.Microbiology spectrum · 2017
    Review
  17. Article
  18. Review
  19. Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 3 institutions in 1 country.

Gilad YaakovCell Signaling Unit, Departament de Ciències Experimentals i de la Salut, Universitat Pompeu Fabra, 08003 Barcelona, Spain.
Alba Duch
María García-Rubio
Josep Clotet
Javier Jimenez
Andrés Aguilera
Francesc Posas
Pompeu Fabra University · ESConsejo Superior de Investigaciones Científicas · ESUniversidad de Sevilla · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

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.

Indexed as

S PhaseBlotting, WesternCell Cycle ProteinsCheckpoint Kinase 2Cyclin BCyclin-Dependent Kinase Inhibitor ProteinsDNA Polymerase IIDNA ReplicationFlow CytometryG1 PhaseG2 PhaseImmunoprecipitationMitogen-Activated Protein KinasesMutationOsmotic PressurePhosphorylationCell Cycle ProteinsCheckpoint Kinase 2CLB5 protein, S cerevisiaeCLB6 protein, S cerevisiaeCyclin BCyclin-Dependent Kinase Inhibitor ProteinsDNA Polymerase IIDpb2 protein, S cerevisiaeHOG1 protein, S cerevisiaeHSL1 protein, S cerevisiaeMitogen-Activated Protein KinasesProtein Serine-Threonine KinasesProtein-Tyrosine KinasesRAD53 protein, S cerevisiaeSaccharomyces cerevisiae ProteinsSIC1 protein, S cerevisiaeSLD2 protein, S cerevisiaeSWE1 protein, S cerevisiae

Identifiers

PMID19477922
PMCPMC2719575
OpenAlexW2154622711

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.