Journal of Bacteriology, January 2001, p. 745-751, Vol. 183, No. 2
0021-9193/01/$04.00+0 DOI: 10.1128/JB.183.2.745-751.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.
Department of Biotechnology, Graduate School of Engineering, Osaka University, Suita, Osaka 565-0871, Japan
Received 17 July 2000/Accepted 13 October 2000
Fatty acid desaturation catalyzed by fatty acid desaturases
requires molecular oxygen (O2). Saccharomyces
cerevisiae cells derepress expression of OLE1
encoding
9 fatty acid desaturase under hypoxic conditions to allow
more-efficient use of limited O2. It has been proposed that
aerobic conditions lead to repression of OLE1 by
well-established O2-responsive repressor Rox1p, since putative binding sequences for Rox1p are present in the promoter of
OLE1. However, we revealed in this study that disruption of ROX1 unexpectedly did not affect the O2
repression of OLE1, indicating that a Rox1p-independent
novel mechanism operates for this repression. We identified by promoter
deletion analysis the 50-bp O2-regulated (O2R) element in
the OLE1 promoter approximately 360 bp upstream of the
start codon. Site-directed mutagenesis of the O2R element showed that
the putative binding motif (5'-GATAA-3') for the GATA family of
transcriptional factors is important for O2 repression. Anaerobic derepression of OLE1 transcription was repressed
by unsaturated fatty acids (UFAs), and interestingly the O2R element was responsible for this UFA repression despite not being included within the fatty acid-regulated (FAR) element previously reported. The
fact that such a short 50-bp O2R element responds to both O2 and UFA signals implies that O2 and UFA
signals merge in the ultimate step of the pathways. We discuss the
differential roles of FAR and O2R elements in the transcriptional
regulation of OLE1.
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