Evidence map›Paper›PMID 9135999›Full record

ArticleGenetics1997

Genetic analysis of default mating behavior in Saccharomyces cerevisiae.

R Dorer, C Boone, T Kimbrough, J Kim, L H Hartwell

Open access · bronzeAbstract read
In one paragraph

Article in Genetics, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
2.2field-weighted citation impact, top 11% 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

34 citing papers in PubMed, 57 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Cell biology of yeast zygotes, from genesis to budding.Biochimica et biophysica acta · 2015
    Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Chemical gradients and chemotropism in yeast.Cold Spring Harbor perspectives in biology · 2009
    Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. The BAR domain proteins: molding membranes in fission, fusion, and phagy.Microbiology and molecular biology reviews : MMBR · 2006
    Review
  17. Article
  18. Article
  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

5 authors at 2 institutions in 2 countries.

R DorerFred Hutchinson Cancer Research Center, Seattle, Washington 98104, USA.
C Boone
T Kimbrough
J Kim
L H Hartwell
Fred Hutch Cancer Center · USSimon Fraser University · CA

Funding

University of Washington Medical Scientist Training Program: MD/PhDT32GM007266 · NIGMS · UNIVERSITY OF WASHINGTON · PI HORWITZ, MARSHALL S. · 1985 to 2023
$30.4M
TRAINING PROGRAM IN GENETICS GENERAL AND MEDICALT32GM007735 · NIGMS · UNIVERSITY OF WASHINGTON · PI THOMAS, JAMES H · 1985 to 2009
$3.8M
GENETIC ANALYSIS OF THE EUKARYOTIC CELL CYCLER01GM017709 · NIGMS · UNIVERSITY OF WASHINGTON · PI HARTWELL, LELAND H · 1985 to 2005
$2.3M
GENETIC ANALYSIS OF THE EUKARYOTIC CELL CYCLER37GM017709 · NIGMS · UNIVERSITY OF WASHINGTON · PI HARTWELL, LELAND H · 1990 to 2000
$534k
NIGMS NIH HHS GM-07266NIGMS NIH HHS GM-17709NIGMS NIH HHS T32 GM07735
6 · The paper itself

Abstract

Haploid Saccharomyces cerevisiae cells find each other during conjugation by orienting their growth toward each other along pheromone gradients (chemotropism). However, when their receptors are saturated for pheromone binding, yeast cells must select a mate by executing a default pathway in which they choose a mating partner at random. We previously demonstrated that this default pathway requires the SPA2 gene. In this report we show that the default mating pathway also requires the AXL1, FUS1, FUS2, FUS3, PEA2, RVS161, and BNI1 genes. These genes, including SPA2, are also important for efficient cell fusion during chemotropic mating. Cells containing null mutations in these genes display defects in cell fusion that subtly affect mating efficiency. In addition, we found that the defect in default mating caused by mutations in SPA2 is partially suppressed by multiple copies of two genes, FUS2 and MFA2. These findings uncover a molecular relationship between default mating and cell fusion. Moreover, because axl1 mutants secrete reduced levels of a-factor and are defective at both cell fusion and default mating, these results reveal an important role for a-factor in cell fusion and default mating. We suggest that default mating places a more stringent requirement on some aspects of cell fusion than does chemotropic mating.

Indexed as

DNA-Binding ProteinsRepressor ProteinsSaccharomyces cerevisiae ProteinsGenes, FungalMutationSaccharomyces cerevisiaeTranscription FactorsASH1 protein, S cerevisiaeDNA-Binding ProteinsRepressor ProteinsSaccharomyces cerevisiae ProteinsTranscription Factors

Identifiers

PMID9135999
PMCPMC1207953
OpenAlexW2172041644

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.