Bromodomain factor 1 (Bdf1p) is a transcriptional regulator. The absence of Bdf1p causes salt sensitivity with abnormal nucleus and mitochondrial dysfunction. In this study, we reported that the salt sensitivity, mitochondrial dysfunction, and nuclear instability of bdf1Δ mutant were suppressed by HDA1 deletion or MEF1 overexpression. Hda1p overexpression inhibited the relieving effects of low-copy overexpression of MEF1. Further analysis showed that Bdf1p regulated HDA1 transcription positively by binding to its promoter at −201 to +6 bp, whereas Hda1p modulated MEF1 expression negatively by binding to its promoter at −201 to +6 bp. These results suggested that Bdf1p likely regulated MEF1 expression negatively by regulating HDA1 positively. Mitochondrial proteomics analysis showed that the expression levels of six mitochondrial proteins were significantly changed by MEF1 overexpression. Among the six genes, over-expression of PDB1, ILV5, or ATP2 partially recovered the salt stress sensitivity of bdf1Δ. However, none of these mitochondrial proteins could recover mitochondrial respiration indicating that the individual functional proteins could not replace Mef1p activity. It indicated that positive regulation of MEF1 was important in recovering the salt sensitivity of bdf1Δ mutant.

• PMID: 25035869
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Journal Article | Research Support, Non-U.S. Gov't

Authors

Chen L, Wang M, Hou J, Liu L, Fu J, Shen Y, Zhang Z, Bao X

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