Open AccessRegulation of S accharomyces cerevisiae MEF1 by H da1p affects salt resistance of bdf1Δ mutant
Author(s) -
Chen Lei,
Wang Mingpeng,
Hou Jin,
Liu Liangyu,
Fu Jiafang,
Shen Yu,
Zhang Zhaojie,
Bao Xiaoming
Publication year - 2014
Publication title -
fems yeast research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.991
H-Index - 92
eISSN - 1567-1364
pISSN - 1567-1356
DOI - 10.1111/1567-1364.12144
Subject(s) - biology , mutant , transcription factor , microbiology and biotechnology , transcriptional regulation , mitochondrion , gene , gene expression , biochemistry
Bromodomain factor 1 ( B df1p) is a transcriptional regulator. The absence of B df1p 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 B df1p regulated HDA1 transcription positively by binding to its promoter at −201 to +6 bp, whereas H da1p modulated MEF1 expression negatively by binding to its promoter at −201 to +6 bp. These results suggested that B df1p 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 M ef1p activity. It indicated that positive regulation of MEF1 was important in recovering the salt sensitivity of bdf1Δ mutant.