Over-expression of the yeast BFR2 gene partially suppresses the growth defects induced by Brefeldin A and by four ER-to-Golgi mutations

Abstract

The fungal metabolite Brefeldin A (BFA) disrupts the Golgi apparatus and its incoming protein flux. We developed a genetic approach to identify yeast proteins involved in the protein transport step that BFA blocks. The BFR2 gene (YDR299W) was thus isolated as a high-copy suppressor of the growth defects induced by BFA in a sensitive strain of Saccharomyces cerevisiae. Although BFR2 over-expression did not cause a secretory block or slow-down, it partially suppressed the growth defect of four mutants blocked at the step of budding or docking of small vesicles en route to the Golgi (sec13-1, sec16-2, sec23-1, ypt1-1). The essential BFR2 gene was predicted to encode an extremely hydrophilic product containing two short regions with potential coiled-coils, one of which corresponds to a cluster of acidic residues.