Yos9, a control protein for misfolded glycosylated and non-glycosylated proteins in ERAD

FEBS Lett. 2011 Oct 3;585(19):3015-9. doi: 10.1016/j.febslet.2011.08.021. Epub 2011 Aug 23.

Abstract

The endoplasmic reticulum (ER) is responsible for folding and delivery of secretory proteins to their site of action. One major modification proteins undergo in this organelle is N-glycosylation. Proteins that cannot fold properly will be directed to a process known as endoplasmic reticulum associated degradation (ERAD). Processing of N-glycans generates a signal for ERAD. The lectin Yos9 recognizes the N-glycan signal of misfolded proteins and acts as a gatekeeper for the delivery of these substrates to the cytoplasm for degradation. Presence of Yos9 accelerates degradation of the glycosylated model ERAD substrate CPY∗. Here we show that Yos9 has also a control function in degradation of the unglycosylated ERAD substrate CPY∗0000. It decelerates its degradation rate.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Carboxypeptidases / genetics
  • Carboxypeptidases / metabolism
  • Carrier Proteins / genetics
  • Carrier Proteins / metabolism*
  • Endoplasmic Reticulum / metabolism*
  • Endoplasmic Reticulum-Associated Degradation / physiology*
  • Glycosylation
  • Mannosidases / genetics
  • Mannosidases / metabolism
  • Protein Folding*
  • Proteins / genetics
  • Proteins / metabolism*
  • Saccharomyces cerevisiae / metabolism
  • Saccharomyces cerevisiae Proteins / genetics
  • Saccharomyces cerevisiae Proteins / metabolism*

Substances

  • Carrier Proteins
  • Proteins
  • Saccharomyces cerevisiae Proteins
  • Yos9 protein, S cerevisiae
  • MNL1 protein, S cerevisiae
  • Mannosidases
  • Carboxypeptidases
  • CPY protein, S cerevisiae