Open AccessMitochondrial dysfunction enhances Gal4‐dependent transcription
Author(s) -
Jeličić Branka,
Traven Ana,
Filić Vedrana,
Sopta Mary
Publication year - 2005
Publication title -
fems microbiology letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.899
H-Index - 151
eISSN - 1574-6968
pISSN - 0378-1097
DOI - 10.1016/j.femsle.2005.09.033
Subject(s) - dna binding domain , mitochondrial dna , biology , cardiolipin , activator (genetics) , transcription (linguistics) , mitochondrial fusion , mitochondrion , transcription factor , promoter , microbiology and biotechnology , mutant , gene expression , gene , biochemistry , phospholipid , linguistics , philosophy , membrane
Mitochondrial dysfunction has been shown to elicit broad effects on nuclear gene expression. We show here that transcription dependent on the prototypical acidic activator Gal4 is responsive to mitochondrial dysfunction. In cells with no mitochondrial DNA, Gal4‐dependent gene expression is elevated. A minimal Gal4 activator containing the DNA binding and activation domain is sufficient for this response. Transcription dependent on a fusion of Gal4 to a heterologous DNA binding domain is similarly elevated in a mitochondrial mutant. Analysis of different Gal4‐dependent promoters and gel mobility shift assays suggest that the effect of mitochondrial dysfunction on Gal4 activity is related to increased DNA binding to the cognate Gal4 element. Given that fermentation is the only means to obtain energy in respiratory deficient cells, it is possible that higher Gal4 activity in cells with dysfunctional mitochondria works to promote more efficient fermentation of galactose.