The yeast SLY gene products, suppressors of defects in the essential GTP-binding Ypt1 protein, may act in endoplasmic reticulum-to-Golgi transport.

摘要: It has been shown previously that defects in the essential GTP-binding protein, Ypt1p, lead to a block protein transport from endoplasmic reticulum (ER) Golgi apparatus yeast Saccharomyces cerevisiae. Here we report four newly discovered suppressors of YPT1 deletion (SLY1-20, SLY2, SLY12, and SLY41) varying degree restore ER-to-Golgi cells lacking Ypt1p. These also partially complement sec21-1 sec22-3 mutants which defect early secretory pathway. Sly1p-depleted cells, as well conditional lethal sly2 null mutant at nonpermissive temperatures, accumulate ER membranes core-glycosylated invertase carboxypeptidase Y. The under restrictive conditions (37 degrees C) can be rescued by multicopy suppressor SLY12 single-copy SLY1-20, indicating these three SLY genes functionally interact. Sly2p is an integral membrane protein.