Protein Variants | Comment | Organism |
---|---|---|
R100W | residue R100 is located near the end of the largest luminal loop between the first two predicted transmembrane segments and is absolutely conserved in all known ALG9 enzymes. Mutation suppresses a dwarf mutant, bri1-9, the phenotypes of which are caused by endoplasmic reticulum retention and endoplasmic reticulum-associated degradation of a brassinosteroid receptor, BRASSINOSTEROID-INSENSITIVE 1, BR1. The mutation prevents the Glc3Man9GlcNAc2 assembly and inhibits the endoplasmic reticulum-associated degradation of bri1-9. Overexpression of EBS4 in the R100W bri1-9 mutant, which encodes the Arabidopsis ortholog of the yeast ALG12 catalyzing the ER luminal alpha1,6 Man addition, adds an alpha1,6 Man to the truncated N-glycan precursor accumulated in R100W bri1-9, promotes the bri1-9 endoplasmic reticulum-associated degradation, and neutralizes the R100W suppressor phenotype | Arabidopsis thaliana |
Organism | UniProt | Comment | Textmining |
---|---|---|---|
Arabidopsis thaliana | A8MR93 | - |
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Synonyms | Comment | Organism |
---|---|---|
ALG12 | - |
Arabidopsis thaliana |
EBS4 | - |
Arabidopsis thaliana |
General Information | Comment | Organism |
---|---|---|
physiological function | overexpression of enzyme in a dwarf mutant, bri1-9, the phenotypes of which are caused by endoplasmic reticulum retention and endoplasmic reticulum-associated degradation of a brassinosteroid receptor, BRASSINOSTEROID-INSENSITIVE 1, and a mutant lacking EBS3 activity, which catalyzes the ER luminal addition of two terminal alpha1,2 mannose residues in assembling the three-branched N-glycan precursor [glucose(Glc)]3(Man)9[N-acetylglucosamine(GlcNAc)]2, adds an alpha1,6-mannose to the truncated N-glycan precursor accumulated in the double mutant, promotes the bri1-9 endoplasmic reticulum-associated degradation, and neutralizes the EBS3 mutant suppressor phenotype | Arabidopsis thaliana |