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The essential Saccharomyces cerevisiae gene BFR2 has been isolated as a high-copy suppressor of the growth defects induced by Brefeldin A, a drug that disrupts the Golgi apparatus and its protein influx. Furthermore, BFR2 has been found to display genetic interactions with four mutations affecting protein transport to the Golgi apparatus. Here we show that the level of BFR2 mRNA rapidly increased over fivefold in response to cold shock, and over threefold following nutrient replenishment by dilution of cells from exhausted to fresh minimal medium. During subsequent growth, the transcript level returned to its basal values, except for a transient drop toward the end of the exponential phase. The early burst of transcription was not caused by toxic compounds in the fresh medium, or by synchrony among cells that had simultaneously entered their first cell cycle. The BFR2 gene product (Bfr2p) was synthesized following the early burst of mRNA, and was no longer produced when the mRNA was back to basal level. Bfr2p was finally degraded after growth became limited, and reached undetectable levels in exhausted medium. Under steady-state conditions of lengthened exponential phase, the intracellular level of Bfr2p remained constant. This peculiar pattern of gene expression suggests that Bfr2p is essential for mass growth or cell proliferation, whereas it is either toxic or not required during nutrient-limited growth.

Expression of the yeast BFR2 gene is regulated at the transcriptional level and through degradation of its product