Genes that allow yeast cells to grow in the absence of the HDEL receptor

• Published in: The EMBO journal Vol. 11; no. 11; pp. 4187 - 4195
• Main Authors: Hardwick, K.G, Boothroyd, J.C, Rudner, A.D, Pelham, H.R.B
• Format: Journal Article
• Language: English
• Published: London Nature Publishing Group 01.11.1992
• Subjects: Amino Acid Sequence; amino acid sequences; Base Sequence; Biological and medical sciences; Cell Membrane - physiology; Cell Membrane - ultrastructure; Classical genetics, quantitative genetics, hybrids; dolichol-p-mannose synthase; embl/x66838; endoplasmic reticulum; erd2 gene; Fundamental and applied biological sciences. Psychology; Fungal Proteins - genetics; Gene Library; gene products; genes; Genes, Fungal; Genes, Suppressor; Genetics of eukaryotes. Biological and molecular evolution; glycoproteins; Golgi apparatus; Golgi Apparatus - physiology; Golgi Apparatus - ultrastructure; HDEL receptor; Intracellular Membranes - physiology; Intracellular Membranes - ultrastructure; ligases; Membrane Glycoproteins - genetics; membrane proteins; Membrane Proteins - genetics; membranes; Molecular Sequence Data; nucleotide sequence; nucleotide sequences; plant proteins; Plasmids; predictions; Protein Sorting Signals - genetics; protein transport; receptors; Receptors, Cell Surface - genetics; Receptors, Cell Surface - physiology; Receptors, Peptide; regulation; Saccharomyces cerevisiae; Saccharomyces cerevisiae - genetics; Saccharomyces cerevisiae - growth & development; Saccharomyces cerevisiae - ultrastructure; Saccharomyces cerevisiae Proteins; SED gene; sed1 gene; sed2 gene; sed3 gene; sed4 gene; structural genes; Thallophyta, bryophyta; Vegetals; Membrane protein; Yeast; Suppressor gene; Retention; Golgi apparatus; Fungi; Proteins; Phenotype; Membrane transport; Deletion; Ascomycetes; Endoplasmic reticulum; Saccharomyces cerevisiae; Thallophyta; Biological receptor
• ISSN: 0261-4189; 1460-2075
• DOI: 10.1002/j.1460-2075.1992.tb05512.x

The ERD2 gene of Saccharomyces cerevisiae encodes the HDEL receptor that sorts ER proteins; it is essential for growth. In the absence of Erd2p the Golgi apparatus is both functionally and morphologically perturbed. Here we describe the isolation of four SED genes (suppressors of the erd2-deletion) which, when present in multiple copies, allow cells to grow in the absence of ERD2. The suppressed strains secrete the ER protein BiP and their internal membranes show a variety of morphological abnormalities. Sequence analysis indicates that all these SED genes encode membrane proteins: SED1 encodes a probable cell surface glycoprotein; SED2 is identical to SEC12, a gene required for the formation of ER-derived transport vesicles; SED4 encodes a protein whose cytoplasmic domain is 45% identical to that of Sec12p; SED3 is DPM1, the structural gene for dolichol-P-mannose synthase. We suggest that the absence of ERD2 causes an imbalance between membrane flow into and out of the Golgi apparatus, and that the SED gene products can compensate for this either by slowing transport from the ER or by stimulating vesicle budding from Golgi membranes.