UMMS Affiliation

Department of Biochemistry and Molecular Pharmacology

Date

3-19-2008

Document Type

Article

Subjects

Gene Expression Regulation, Fungal; Membrane Proteins; Mutation; Protein Biosynthesis; Protein Sorting Signals; Protein Subunits; Protein Transport; Receptors, Cytoplasmic and Nuclear; Receptors, Peptide; Saccharomyces cerevisiae; Saccharomyces cerevisiae Proteins; Signal Recognition Particle; Time Factors

Disciplines

Life Sciences | Medicine and Health Sciences

Abstract

The signal recognition particle (SRP)-dependent targeting pathway facilitates rapid, efficient delivery of the ribosome-nascent chain complex (RNC) to the protein translocation channel. We test whether the SRP receptor (SR) locates a vacant protein translocation channel by interacting with the yeast Sec61 and Ssh1 translocons. Surprisingly, the slow growth and cotranslational translocation defects caused by deletion of the transmembrane (TM) span of yeast SRbeta (SRbeta-DeltaTM) are exaggerated when the SSH1 gene is disrupted. Disruption of the SBH2 gene, which encodes the beta subunit of the Ssh1p complex, likewise causes a growth defect when combined with SRbeta-DeltaTM. Cotranslational translocation defects in the ssh1DeltaSRbeta-DeltaTM mutant are explained by slow and inefficient in vivo gating of translocons by RNCs. A critical function for translocation channel beta subunits in the SR-channel interaction is supported by the observation that simultaneous deletion of Sbh1p and Sbh2p causes a defect in the cotranslational targeting pathway that is similar to the translocation defect caused by deletion of either subunit of the SR.

Rights and Permissions

Citation: J Cell Biol. 2008 Mar 24;180(6):1149-61. Epub 2008 Mar 17. Link to article on publisher's site

DOI of Published Version

10.1083/jcb.200707196

Related Resources

Link to Article in PubMed

Journal Title

The Journal of cell biology

PubMed ID

18347066

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