BST1/YFL025C Summary Help

Standard Name BST1 1
Systematic Name YFL025C
Alias PER17 2
Feature Type ORF, Verified
Description GPI inositol deacylase of the endoplasmic reticulum (ER); negatively regulates COPII vesicle formation; prevents production of vesicles with defective subunits; required for proper discrimination between resident ER proteins and Golgi-bound cargo molecules; functional ortholog of human PGAP1, mutation of which is associated with intellectual disability and encephalopathy (1, 3, 4 and see Summary Paragraph)
Name Description Bypass of Sec Thirteen 1
Chromosomal Location
ChrVI:87234 to 84145 | ORF Map | GBrowse
Note: this feature is encoded on the Crick strand.
Gene Ontology Annotations All BST1 GO evidence and references
  View Computational GO annotations for BST1
Molecular Function
Manually curated
Biological Process
Manually curated
Cellular Component
Manually curated
Regulators 1 genes
Classical genetics
Large-scale survey
399 total interaction(s) for 206 unique genes/features.
Physical Interactions
  • Affinity Capture-MS: 1
  • Affinity Capture-RNA: 1
  • Affinity Capture-Western: 2
  • PCA: 4

Genetic Interactions
  • Dosage Growth Defect: 4
  • Negative Genetic: 274
  • Phenotypic Enhancement: 1
  • Phenotypic Suppression: 33
  • Positive Genetic: 64
  • Synthetic Growth Defect: 11
  • Synthetic Lethality: 1
  • Synthetic Rescue: 3

Expression Summary
Length (a.a.) 1,029
Molecular Weight (Da) 117,754
Isoelectric Point (pI) 6.72
Phosphorylation PhosphoGRID | PhosphoPep Database
sequence information
ChrVI:87234 to 84145 | ORF Map | GBrowse
Note: this feature is encoded on the Crick strand.
Last Update Coordinates: 2011-02-03 | Sequence: 1996-07-31
Subfeature details
Most Recent Updates
Coordinates Sequence
CDS 1..3090 87234..84145 2011-02-03 1996-07-31
Retrieve sequences
Analyze Sequence
S288C only
S288C vs. other species
S288C vs. other strains
External Links All Associated Seq | E.C. | Entrez Gene | Entrez RefSeq Protein | MIPS | Search all NCBI (Entrez) | UniProtKB
Primary SGDIDS000001869

Bst1p is a glycosylphosphatidylinositol (GPI) inositol deacylase that mediates inositol deacylation of GPI-anchored proteins, which may be required for their efficient incorporation into COPII transport vesicles through association with cargo receptors (3). An integral membrane protein that resides predominantly in the endoplasmic reticulum (ER), Bst1p negatively regulates COPII vesicle formation, preventing the production of vesicles with defective or missing subunits (2). Bst1p is also required for proper discrimination between resident ER proteins and Golgi-bound cargo molecules (1), and is required for the transport of misfolded proteins to the Golgi, though dispensable for the transport of many normal cargo proteins (2). Bst1p also plays a role in the retrieval to the ER of proteins transported to the Golgi apparatus via COPII-coated vesicles. Bst1p thus represents a novel class of ER proteins that link the regulation of vesicle coat assembly to cargo sorting (1). Null mutations in BST1 suppress mutations in the essential COPII gene SEC13, which is important for the formation of ER to Golgi transport vesicles (1).

Last updated: 2004-11-02 Contact SGD

References cited on this page View Complete Literature Guide for BST1
1) Elrod-Erickson MJ and Kaiser CA  (1996) Genes that control the fidelity of endoplasmic reticulum to Golgi transport identified as suppressors of vesicle budding mutations. Mol Biol Cell 7(7):1043-58
2) Vashist S, et al.  (2001) Distinct retrieval and retention mechanisms are required for the quality control of endoplasmic reticulum protein folding. J Cell Biol 155(3):355-68
3) Tanaka S, et al.  (2004) Inositol deacylation of glycosylphosphatidylinositol-anchored proteins is mediated by mammalian PGAP1 and yeast Bst1p. J Biol Chem 279(14):14256-63
4) Murakami Y, et al.  (2014) Null mutation in PGAP1 impairing Gpi-anchor maturation in patients with intellectual disability and encephalopathy. PLoS Genet 10(5):e1004320