Interplay between BDF1 and BDF2 and their roles in regulating the yeast salt stress response

The homologous genes BDF1 and BDF2 in S accharomyces cerevisiae encode bromodomain‐containing transcription factors. Although double deletion of BDF1 and BDF2 is lethal, single deletion does not affect cell viability. The bdf2∆ cells showed normal growth upon salt stress. However, the absence of Bdf1p resulted in a salt‐sensitive phenotype, and the salt sensitivity was suppressed by overexpression of BDF2 . In this study, we further demonstrated that BDF2 shows dosage compensation in suppressing the salt sensitivity of bdf1∆ . None of the tested domains replaced the function of intact B df1p. The 494–626 region in B df1p was more important than the other domains for salt resistance. In addition, B df1p negatively regulated the expression of BDF2 by binding its promoter at loci −387 to −48. However, B df2p did not affect the expression of BDF1 . In addition, B df1p and its defective functional domain mutants could combine with B df2p. This physical interaction increased the salt tolerance of bdf1∆ . The mitochondrial dysfunctions caused by BDF1 deletion were restored by overexpression of BDF2 under salt stress conditions. Structured digital abstractBDF2 physically interacts with BDF1 by anti tag coimmunoprecipitation ( View interaction ) BDF2 physically interacts with BDF1 by pull down ( View interaction )