Evidence map›Paper›PMID 15456892›Full record

ArticleMolecular and cellular biology2004

Persistent activation by constitutive Ste7 promotes Kss1-mediated invasive growth but fails to support Fus3-dependent mating in yeast.

Seth Maleri, Qingyuan Ge, Elizabeth A Hackett, Yuqi Wang, Henrik G Dohlman, Beverly Errede

Abstract read
In one paragraph

Article in Molecular and cellular biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.7field-weighted citation impact, top 18% 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

26 citing papers in PubMed, 57 citations in OpenAlex.

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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 1 institution in 1 country.

Seth MaleriDepartment of Biochemistry and Biophysics, CB 7260, 512 ME Jones, University of North Carolina, Chapel Hill, NC 27599-7260, USA.
Qingyuan Ge
Elizabeth A Hackett
Yuqi Wang
Henrik G Dohlman
Beverly Errede
University of North Carolina at Chapel Hill · US

Funding

REGULATORS OF G PROTEIN SIGNALING IN YEASTR01GM059167 · NIGMS · YALE UNIVERSITY · PI DOHLMAN, HENRIK G. · 1999 to 2015
$3.7M
KINASES AND CONTROL OF CELL-TYPE SPECIALIZATIONR01GM039852 · NIGMS · UNIVERSITY OF NORTH CAROLINA CHAPEL HILL · PI ERREDE, BEVERLY · 1988 to 2002
$900k
CLASSIFICATION AND CODING OF ADVERSE DRUG REACTIONSR43GM050591 · NIGMS · BELMONT RESEARCH, INC. · PI ONG, JAMES C · 1995 to 1995
–
CLASSIFICATION AND CODING OF ADVERSE DRUG REACTIONSR44GM050591 · NIGMS · BELMONT RESEARCH, INC. · PI JOHNSTON, MICHAEL F · 1997 to 1998
–
NIGMS NIH HHS GM39852NIGMS NIH HHS GM5059167NIGMS NIH HHS R01 GM059167
6 · The paper itself

Abstract

Mitogen-activated protein kinase kinase kinase-Ste11 (MAPKKK-Ste11), MAPKK-Ste7, and MAPK-Kss1 mediate pheromone-induced mating differentiation and nutrient-responsive invasive growth in Saccharomyces cerevisiae. The mating pathway also requires the scaffold-Ste5 and the additional MAPK-Fus3. One contribution to specificity in this system is thought to come from stimulus-dependent recruitment of the MAPK cascade to upstream activators that are unique to one or the other pathway. To test this premise, we asked if stimulus-independent signaling by constitutive Ste7 would lead to a loss of biological specificity. Instead, we found that constitutive Ste7 promotes invasion without supporting mating responses. This specificity occurs because constitutive Ste7 activates Kss1, but not Fus3, in vivo and promotes filamentation gene expression while suppressing mating gene expression. Differences in the ability of constitutive Ste7 variants to bind the MAPKs and Ste5 account for the selective activation of Kss1. These findings support the model that Fus3 activation in vivo requires binding to both Ste7 and the scaffold-Ste5 but that Kss1 activation is independent of Ste5. This scaffold-independent activation of Kss1 by constitutive Ste7 and the existence of mechanisms for pathway-specific promoter discrimination impose a unique developmental fate independently of any distinguishing external stimuli.

Indexed as

Adaptor Proteins, Signal TransducingEnzyme ActivationFeedback, PhysiologicalGene Expression Regulation, FungalGenes, ReporterIsoenzymesMAP Kinase Signaling SystemMitogen-Activated Protein Kinase KinasesMitogen-Activated Protein KinasesPhenotypePheromonesPhosphorylationProtein KinasesRecombinant Fusion ProteinsSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsAdaptor Proteins, Signal TransducingFUS3 protein, S cerevisiaeIsoenzymesKSS1 protein, S cerevisiaeMitogen-Activated Protein Kinase KinasesMitogen-Activated Protein KinasesPheromonesProtein KinasesRecombinant Fusion ProteinsSaccharomyces cerevisiae ProteinsSTE5 protein, S cerevisiaeSTE7 protein, S cerevisiaeUbiquitin

Identifiers

PMID15456892
PMCPMC517903
OpenAlexW2013134990

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.