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Transition metal induction of the S. cerevisiae OLE1 gene occurs through multiple promoter elements.
Author(s) -
Mintz Jason D,
Oh ChanSeok,
Martin Charles
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.807.15
Subject(s) - transcription (linguistics) , biology , transcription factor , mutant , cobalt , chemistry , gene , microbiology and biotechnology , biochemistry , inorganic chemistry , philosophy , linguistics
The S. cerevisiae Δ‐9 fatty acid desaturase, encoded by the OLE1 gene, converts saturated fatty acyl CoA to monounsaturated species. Hypoxia and transition metals, such as cobalt, induce OLE1 expression. Expression of OLE1 is dependent on two ER membrane proteins, Spt23p and Mga2p, that appear to serve as co‐transcription activators of OLE1, however, hypoxic and cobalt induction of OLE1 appear to be controlled only through Mga2p. The OLE1 promoter contains two regions essential for transcription activation. The FAR region activates transcription under normoxic conditions whereas the downstream LORE element is essential for the hypoxic stimulation of OLE1 expression under Mga2p activation. This study examines the role of cobalt on the Mga2p induction of OLE1 through the FAR and LORE promoter elements. In ( spt23;MGA2 ) cells, cobalt causes a 25‐fold induction of the full promoter. Mutations in either the LORE or FAR region produce low, but cobalt‐inducible levels of reporter activity indicating that the two elements act in response to cobalt in a differential manner. Cobalt has been proposed to be linked through the hypoxic induction of OLE1 via its inhibition of a mitochondrial cytochrome dependent signal transduction pathway. Analysis of respiratory deficient mutants shows a strong cobalt activation of OLE1, however, suggesting that there may be more than one pathway for induction of the gene.