Preparing your results

Our searching services are busy right now. Your search will reload in five seconds.

X
Forgot Password

If you have forgotten your password you can enter your email here and get a temporary password sent to your email.

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

The FEBS journal | May 25, 2013

http://www.ncbi.nlm.nih.gov/pubmed/23452060

The homologous genes BDF1 and BDF2 in Saccharomyces 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 Bdf1p. The 494-626 region in Bdf1p was more important than the other domains for salt resistance. In addition, Bdf1p negatively regulated the expression of BDF2 by binding its promoter at loci -387 to -48. However, Bdf2p did not affect the expression of BDF1. In addition, Bdf1p and its defective functional domain mutants could combine with Bdf2p. 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.

Pubmed ID: 23452060 RIS Download

Mesh terms: Apoptosis | Base Sequence | Cell Nucleus | Dosage Compensation, Genetic | Gene Expression Regulation, Fungal | Gene Knockout Techniques | Microbial Viability | Mitochondria | Promoter Regions, Genetic | Protein Binding | Protein Structure, Tertiary | Saccharomyces cerevisiae | Saccharomyces cerevisiae Proteins | Salt-Tolerance | Stress, Physiological | TATA Box | Transcription Factors

Research resources used in this publication

None found

Research tools detected in this publication

None found

Data used in this publication

None found

Associated grants

None

Publication data is provided by the National Library of Medicine ® and PubMed ®. Data is retrieved from PubMed ® on a weekly schedule. For terms and conditions see the National Library of Medicine Terms and Conditions.