Evidence map›Paper›PMID 10880465›Full record

ArticleGenetics2000

Defects in protein glycosylation cause SHO1-dependent activation of a STE12 signaling pathway in yeast.

P J Cullen, J Schultz, J Horecka, B J Stevenson, Y Jigami, G F Sprague

Open access · bronzeAbstract read
In one paragraph

Article in Genetics, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

60 citing papers in PubMed, 121 citations in OpenAlex.

  1. Article
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  5. Contribution ofInfection and drug resistance · 2023
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  10. Deletion ofFrontiers in microbiology · 2019
    Article
  11. Impact of Fungal MAPK Pathway Targets on the Cell Wall.Journal of fungi (Basel, Switzerland) · 2018
    Article
  12. Article
  13. Spatial landmarks regulate a Cdc42-dependent MAPK pathway to control differentiation and the response to positional compromise.Proceedings of the National Academy of Sciences of the United States of America · 2016
    Article
  14. Article
  15. Article
  16. Article
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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

6 authors at 2 institutions in 2 countries.

P J CullenInstitute of Molecular Biology, University of Oregon, Eugene, Oregon 97403-1229, USA. gsprague@molbio.uoregon.edu
J Schultz
J Horecka
B J Stevenson
Y Jigami
G F Sprague
University of Oregon · USNational Institute of Advanced Industrial Science and Technology · JP

Funding

GENETIC REGULATION OF YEAST CELL TYPER01GM030027 · NIGMS · UNIVERSITY OF OREGON · PI SPRAGUE, GEORGE F. · 1985 to 2008
$3.0M
NEGATIVE REGULATORS OF YEAST PHEROMONE RESPONSE PATHWAYF32GM019188 · NIGMS · UNIVERSITY OF OREGON · PI CULLEN, PAUL J · 1998 to 2000
$39k
GENETICS OF SIGNAL TRANSDUCTIONF32GM014591 · NIGMS · UNIVERSITY OF OREGON · PI SCHULTZ, JANET L · 1991 to 1993
–
NIGMS NIH HHS GM14591NIGMS NIH HHS GM19188NIGMS NIH HHS GM-30027
6 · The paper itself

Abstract

In haploid Saccharomyces cerevisiae, mating occurs by activation of the pheromone response pathway. A genetic selection for mutants that activate this pathway uncovered a class of mutants defective in cell wall integrity. Partial loss-of-function alleles of PGI1, PMI40, PSA1, DPM1, ALG1, MNN10, SPT14, and OCH1, genes required for mannose utilization and protein glycosylation, activated a pheromone-response-pathway-dependent reporter (FUS1) in cells lacking a basal signal (ste4). Pathway activation was suppressed by the addition of mannose to hexose isomerase mutants pgi1-101 and pmi40-101, which bypassed the requirement for mannose biosynthesis in these mutants. Pathway activation was also suppressed in dpm1-101 mutants by plasmids that contained RER2 or PSA1, which produce the substrates for Dpm1. Activation of FUS1 transcription in the mannose utilization/protein glycosylation mutants required some but not all proteins from three different signaling pathways: the pheromone response, invasive growth, and HOG pathways. We specifically suggest that a Sho1 --> Ste20/Ste50 --> Ste11 --> Ste7 --> Kss1 --> Ste12 pathway is responsible for activation of FUS1 transcription in these mutants. Because loss of pheromone response pathway components leads to a synthetic growth defect in mannose utilization/protein glycosylation mutants, we suggest that the Sho1 --> Ste12 pathway contributes to maintenance of cell wall integrity in vegetative cells.

Indexed as

GlycosylationSaccharomyces cerevisiae ProteinsCell WallFungal ProteinsGenetic Complementation TestMannoseMembrane GlycoproteinsMembrane ProteinsMitogen-Activated Protein KinasesMutationPheromonesPromoter Regions, GeneticProtein Kinase CRecombinant Fusion ProteinsSaccharomyces cerevisiaeSignal TransductionFungal ProteinsFUS1 protein, S cerevisiaeGAS1 protein, S cerevisiaeHOG1 protein, S cerevisiaeMannoseMembrane GlycoproteinsMembrane ProteinsMitogen-Activated Protein KinasesPheromonesProtein Kinase CRecombinant Fusion ProteinsSaccharomyces cerevisiae ProteinsSTE12 protein, S cerevisiaeTranscription Factors

Identifiers

PMID10880465
PMCPMC1461155
OpenAlexW2142189742

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.