SUP35/YDR172W Summary

Standard Name	SUP35 (see Nomenclature conflict Note)
Systematic Name	YDR172W
Alias	GST1 , PNM2 1 , SAL3 , SUF12 , SUP2 , SUP36
Feature Type	ORF, Verified
Description	Translation termination factor eRF3, has a role in mRNA deadenylation and decay; altered protein conformation creates the [PSI(+)] prion that alters translational fidelity and results in a nonsense suppressor phenotype (2, 3, 4, 5 and see Summary Paragraph) Also known as: [PSI] , [PSI(+)]
Name Description	SUPpressor
Gene Product Alias	eRF3

Chromosomal Location	ChrIV:808324 to 810381 \| ORF Map \| GBrowse

	Genetic position: 142.87 cM

Gene Ontology Annotations All SUP35 GO evidence and references

	View Computational GO annotations for SUP35
Molecular Function
Manually curated	translation release factor activity (IDA)
Biological Process
Manually curated	nuclear-transcribed mRNA catabolic process, deadenylation-dependent decay (IMP, IPI) translational termination (IDA)
Cellular Component
Manually curated	cytosol (TAS) translation release factor complex (IDA)

Mutant phenotypes All SUP35 Phenotype evidence and references

Classical genetics
conditional	budding index: increased heat sensitivity: increased
Large-scale survey
null	haploinsufficient inviable
reduction of function	colony sectoring: increased competitive fitness: normal
Resources	PROPHECY \| PhenoM \| SCMD \| ScreenTroll \| Yeast Fitness Database

interactions All SUP35 Interaction evidence and references

	368 total interaction(s) for 235 unique genes/features.
Physical Interactions	Affinity Capture-MS: 57 Affinity Capture-RNA: 4 Affinity Capture-Western: 34 Biochemical Activity: 2 Co-crystal Structure: 5 Co-localization: 2 Co-purification: 2 Protein-peptide: 1 Reconstituted Complex: 41 Two-hybrid: 18
Genetic Interactions	Dosage Growth Defect: 1 Dosage Lethality: 7 Dosage Rescue: 9 Negative Genetic: 35 Phenotypic Enhancement: 9 Phenotypic Suppression: 42 Positive Genetic: 82 Synthetic Growth Defect: 6 Synthetic Lethality: 2 Synthetic Rescue: 9
Resources	BioGRID \| BOND \| BioPIXIE \| CYC2008 (complexes) \| Complexome \| DIP \| DRYGIN \| GeneMANIA \| InterologFinder

Expression Summary


Resources	Expression Summary \| Cell cycle and metabolic oscillation \| Cell cycle transcript profile \| Cyclebase \| Genevestigator \| GermOnline \| SPELL \| YMGV \| YeastFunc

Protein Information All SUP35 Protein evidence and references

Localization	YeastRC \| YPL+ \| YeastGFP
Phosphorylation	PhosphoGRID \| PhosphoPep Database
Structure	GPMDB \| SCOP \| YeastRC
Homologs	Ashbya (AGD) \| CGD Homologs \| CandidaDB Homologs \| Fungal Orthogroups Repository \| P-POD \| PDB Homologs \| PhylomeDB \| YGOB \| YOGY

sequence information

ChrIV:808324 to 810381 | |

: 142.87 cM

Last Update

Coordinates: 2011-02-03 | Sequence: 1996-07-31

Subfeature details

	Relative Coordinates	Chromosomal Coordinates	Most Recent Updates
	Relative Coordinates	Chromosomal Coordinates	Coordinates	Sequence
CDS	1..2058	808324..810381	2011-02-03	1996-07-31

Retrieve sequences

Analyze Sequence

S288C only	BLASTP \| ATCC/WashU Clones \| BLASTN \| Design Primers \| Restriction Fragment Map \| Restriction Fragment Sizes \| Six-Frame Translation
S288C vs. other species	Fungal Alignment \| BLASTN vs. fungi \| BLASTP at NCBI \| BLASTP vs. fungi \| Synteny Viewer
S288C vs. other strains	Strain Alignment

Resources

External Links	All Associated Seq \| Entrez Gene \| Entrez RefSeq Protein \| MIPS \| Search all NCBI (Entrez) \| UniProtKB

Primary SGDID	S000002579

NOMENCLATURE CONFLICT NOTE

Name	Relevance	Description
SUP2	Nomenclature conflict	SUP2 has been used to refer to both SUP35/YDR172W, which encodes a translation release factor, and SUP2/tY(GUA)D, which encodes tRNA-Tyr.

SUMMARY PARAGRAPH for SUP35

The [PSI+] prion determinant causes nonsense suppressor phenotype due to a reduced function of the translation termination factor Sup35p (eRF3) polymerized into amyloid fibrils. Prion state of the Rnq1 protein, [PIN+], is required for the [PSI+] de novo generation, but not propagation. Yeast [psi-] [PIN+] cells overproducing Sup35p can exhibit nonsense suppression without generation of a stable [PSI+]. In such cells most of Sup35p is present in amyloid polymers, though remaining Sup35p monomer is sufficient for normal translation termination. Presence of these polymers strictly depends on [PIN+], suggesting that their maintenance relies on efficient generation de novo, rather than inheritance. Sup35p polymers contain Rnq1p, confirming that Rnq1p polymers seed Sup35p polymerization (4).

Last updated: 2005-03-15

References cited on this page View Complete Literature Guide for SUP35

1)	Doel SM, et al. (1994) The dominant PNM2- mutation which eliminates the psi factor of Saccharomyces cerevisiae is the result of a missense mutation in the SUP35 gene. Genetics 137(3):659-70
2)	Lindquist S, et al. (2001) Investigating protein conformation-based inheritance and disease in yeast. Philos Trans R Soc Lond B Biol Sci 356(1406):169-76
3)	Derkatch IL, et al. (2004) Effects of Q/N-rich, polyQ, and non-polyQ amyloids on the de novo formation of the [PSI+] prion in yeast and aggregation of Sup35 in vitro. Proc Natl Acad Sci U S A 101(35):12934-9
4)	Salnikova AB, et al. (2005) Nonsense suppression in yeast cells overproducing Sup35 (eRF3) is caused by its non-heritable amyloids. J Biol Chem 280(10):8808-12
5)	Funakoshi Y, et al. (2007) Mechanism of mRNA deadenylation: evidence for a molecular interplay between translation termination factor eRF3 and mRNA deadenylases. Genes Dev 21(23):3135-48