Evidence map›Paper›PMID 30921326›Full record

ArticlePLoS genetics2019

The p38/HOG stress-activated protein kinase network couples growth to division in Candida albicans.

Adnane Sellam, Julien Chaillot, Jaideep Mallick, Faiza Tebbji, Julien Richard Albert, Michael A Cook, Mike Tyers

Abstract read
In one paragraph

Article in PLoS genetics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
–field-weighted citation impact
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

22 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Physiological adventures inMicrobiology and molecular biology reviews : MMBR · 2024
    Review
  7. Article
  8. Article
  9. Article
  10. The Role of Sfp1 inJournal of fungi (Basel, Switzerland) · 2022
    Article
  11. Article
  12. Article
  13. What programs the size of animal cells?Frontiers in cell and developmental biology · 2022
    Review
  14. Article
  15. Article
  16. Review
  17. AJournal of fungi (Basel, Switzerland) · 2021
    Article
  18. DNA damage checkpoint and repair: From the budding yeastComputational and structural biotechnology journal · 2021
    Review
  19. Article
  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.

Adnane SellamInfectious Diseases Research Centre (CRI), CHU de Québec Research Center (CHUQ), Université Laval, Quebec City, QC, Canada.ORCID 0000-0002-0506-7752
Julien ChaillotInfectious Diseases Research Centre (CRI), CHU de Québec Research Center (CHUQ), Université Laval, Quebec City, QC, Canada.
Jaideep MallickInstitute for Research in Immunology and Cancer (IRIC), Department of Medicine, Université de Montréal, Montréal, Québec, Canada.
Faiza TebbjiInfectious Diseases Research Centre (CRI), CHU de Québec Research Center (CHUQ), Université Laval, Quebec City, QC, Canada.
Julien Richard AlbertDepartment of Medical Genetics, University of British Columbia, Vancouver, British Columbia, Canada.
Michael A CookCentre for Systems Biology, Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, Toronto, Canada.
Mike TyersInstitute for Research in Immunology and Cancer (IRIC), Department of Medicine, Université de Montréal, Montréal, Québec, Canada.ORCID 0000-0002-9713-9994

Funding

BioGRID: an open resource for biological interactions and network analysisR01RR024031 · NCRR · SINAI HEALTH SYSTEM · PI TYERS, MIKE · 2007 to 2011
$3.2M
NCRR NIH HHS R01 RR024031
6 · The paper itself

Abstract

Cell size is a complex trait that responds to developmental and environmental cues. Quantitative size analysis of mutant strain collections disrupted for protein kinases and transcriptional regulators in the pathogenic yeast Candida albicans uncovered 66 genes that altered cell size, few of which overlapped with known size genes in the budding yeast Saccharomyces cerevisiae. A potent size regulator specific to C. albicans was the conserved p38/HOG MAPK module that mediates the osmostress response. Basal HOG activity inhibited the SBF G1/S transcription factor complex in a stress-independent fashion to delay the G1/S transition. The HOG network also governed ribosome biogenesis through the master transcriptional regulator Sfp1. Hog1 bound to the promoters and cognate transcription factors for ribosome biogenesis regulons and interacted genetically with the SBF G1/S machinery, and thereby directly linked cell growth and division. These results illuminate the evolutionary plasticity of size control and identify the HOG module as a nexus of cell cycle and growth regulation.

Indexed as

Candida albicansCell CycleCell DivisionCell SizeGene Expression Regulation, FungalMitogen-Activated Protein Kinasesp38 Mitogen-Activated Protein KinasesPhosphorylationSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsSignal TransductionTranscription FactorsHOG1 protein, S cerevisiaeMitogen-Activated Protein Kinasesp38 Mitogen-Activated Protein KinasesSaccharomyces cerevisiae ProteinsTranscription Factors

Identifiers

PMID30921326
PMCPMC6456229

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.