Evidence map›Paper›PMID 26640955›Full record

ArticlePLoS genetics2015

Stable Pseudohyphal Growth in Budding Yeast Induced by Synergism between Septin Defects and Altered MAP-kinase Signaling.

Junwon Kim, Mark D Rose

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.8field-weighted citation impact, top 27% 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

10 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Exocyst subunitJournal of biosciences · 2020
    Article
  8. Article
  9. Article
  10. Review
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

2 authors at 1 institution in 1 country.

Junwon KimDepartment of Molecular Biology, Princeton University, Princeton, New Jersey, United States of America.
Mark D RoseDepartment of Molecular Biology, Princeton University, Princeton, New Jersey, United States of America.
Princeton University · US

Funding

Mechanisms of Nuclear and Cell Fusion in YeastR01GM037739 · NIGMS · PRINCETON UNIVERSITY · PI ROSE, MARK DAVID · 1987 to 2016
$7.4M
NIGMS NIH HHS GM037739NIGMS NIH HHS R01 GM037739
6 · The paper itself

Abstract

Upon nutrient limitation, budding yeasts like Saccharomyces cerevisiae can be induced to adopt alternate filament-like growth patterns called diploid pseudohyphal or invasive haploid growth. Here, we report a novel constitutive pseudohyphal growth state, sharing some characteristics with classic forms of filamentous growth, but differing in crucial aspects of morphology, growth conditions and genetic regulation. The constitutive pseudohyphal state is observed in fus3 mutants containing various septin assembly defects, which we refer to as sadF growth (septin assembly defect induced filamentation) to distinguish it from classic filamentation pathways. Similar to other filamentous states, sadF cultures comprise aggregated chains of highly elongated cells. Unlike the classic pathways, sadF growth occurs in liquid rich media, requiring neither starvation nor the key pseudohyphal proteins, Flo8p and Flo11p. Moreover sadF growth occurs in haploid strains of S288C genetic background, which normally cannot undergo pseudohyphal growth. The sadF cells undergo highly polarized bud growth during prolonged G2 delays dependent on Swe1p. They contain septin structures distinct from classical pseudo-hyphae and FM4-64 labeling at actively growing tips similar to the Spitzenkörper observed in true hyphal growth. The sadF growth state is induced by synergism between Kss1p-dependent signaling and septin assembly defects; mild disruption of mitotic septins activates Kss1p-dependent gene expression, which exacerbates the septin defects, leading to hyper-activation of Kss1p. Unlike classical pseudo-hyphal growth, sadF signaling requires Ste5, Ste4 and Ste18, the scaffold protein and G-protein β and γ subunits from the pheromone response pathway, respectively. A swe1 mutation largely abolished signaling, breaking the positive feedback that leads to amplification of sadF signaling. Taken together, our findings show that budding yeast can access a stable constitutive pseudohyphal growth state with very few genetic and regulatory changes.

Indexed as

Cell CycleCell Cycle ProteinsCell DivisionGene Expression Regulation, FungalHaploidyHyphaeMAP Kinase Signaling SystemMembrane GlycoproteinsMitogen-Activated Protein KinasesMutationNuclear ProteinsProtein-Tyrosine KinasesSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsSeptinsTrans-ActivatorsCell Cycle ProteinsFLO11 protein, S cerevisiaeFLO8 protein, S cerevisaieFUS3 protein, S cerevisiaeKSS1 protein, S cerevisiaeMembrane GlycoproteinsMitogen-Activated Protein KinasesNuclear ProteinsProtein-Tyrosine KinasesSaccharomyces cerevisiae ProteinsSeptinsSWE1 protein, S cerevisiaeTrans-Activators

Identifiers

PMID26640955
PMCPMC4671653
OpenAlexW2193661360

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.