Phenotype Help

STE14 / YDR410C Phenotype

Phenotype annotations for a gene are curated single mutant phenotypes that require an observable (e.g., "cell shape"), a qualifier (e.g., "abnormal"), a mutant type (e.g., null), strain background, and a reference. In addition, annotations are classified as classical genetics or high-throughput (e.g., large scale survey, systematic mutation set). Whenever possible, allele information and additional details are provided.


Summary
Non-essential gene; null mutant of ‘a’ mating type is sterile; null mutant fails to methylate a-factor, Ras1p, or Ras2p; null mutant displays defective export of a-factor; overexpression causes proliferation of the nuclear inner membrane; in large-scale studies, null mutation confers shorter chronological lifespan and sensitivity to myriocin and CG-1521; diploid heterozygous null mutant is sensitive to starvation

Annotations

A phenotype is defined as an observable (e.g., apoptosis) and a qualifier (e.g., increased). There may be more than one row with the same phenotype if that phenotype was observed in separate studies or in different conditions, strains, alleles, etc.

20 entries for 15 phenotypes


Increase the total number of rows showing on this page using the pull-down located below the table, or use the page scroll at the table's top right to browse through the table's pages; use the arrows to the right of a column header to sort by that column; filter the table using the "Filter" box at the top of the table; click on the small "i" buttons located within a cell for an annotation to view further details.

PhenotypeExperiment TypeMutant InformationStrain BackgroundChemicalDetailsReference
chemical compound accumulation: abnormal
systematic mutation setnull
Allele: ste14-Δ
S288C alpha-amino acidDetails: Significantly altered free amino acid profile (X^2- test adjusted p < 0.01), showing 2 simultaneous amino acid changes (Z-test, adjusted p < 0.01)
Mülleder M, et al. (2016) PMID:27693354
chemical compound accumulation: decreased
systematic mutation setnull
Allele: ste14-Δ
S288C serineMülleder M, et al. (2016) PMID:27693354
chemical compound accumulation: decreased
systematic mutation setnull
Allele: ste14-Δ
S288C threonineMülleder M, et al. (2016) PMID:27693354
chronological lifespan: decreased
systematic mutation setnull
Allele: ste14-Δ
S288CMarek A and Korona R (2013) PMID:24151994
haploproficient
heterozygous diploid, competitive growth

genome-wide fitness profiling

null
Allele: ste14-Δ
S288CMedia: turbidostat growth in FPM medium
Details: Relative growth score: 0.0094
Pir P, et al. (2012) PMID:22244311
mating response: abnormal
classical geneticsunspecifiedOtherDetails: a-specific sterile
Wilson KL and Herskowitz I (1987) PMID:3552875
mating response: absent
classical geneticsnull
Allele: ste14-Δ
OtherHuyer G, et al. (2006) PMID:16963638
nuclear morphology: abnormal
classical geneticsoverexpressionOtherDetails: proliferation of the inner nuclear membrane, characteristic for overproduction of inner membrane proteins
Barrowman J, et al. (2008) PMID:18923140
oxidative stress resistance: decreased
competitive growth null
Allele: ste14-Δ
S288C1 mM paraquatHelsen J, et al. (2020) PMID:32658971
pheromone production: decreased
classical geneticsnull
Allele: ste14-Δ
OtherDetails: export of a-factor is defective
Sapperstein S, et al. (1994) PMID:8289819
Showing 1 to 10 of 20 entries

Shared Phenotypes

This diagram displays phenotype observables (purple squares) that are shared between the given gene (yellow circle) and other genes (gray circles) based on the number of phenotype observables shared (adjustable using the slider at the bottom).


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Click on a gene or phenotype observable name to go to its specific page within SGD; drag any of the gene or observable objects around within the visualization for easier viewing; click “Reset” to automatically redraw the diagram; filter the genes that share observable terms with the given gene by the number of terms they share by clicking anywhere on the slider bar or dragging the tab to the desired filter number.


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