Abstract
We examined the effects of unsaturated fatty acid (UFA) species and their concentration on the expression ofOLE1,which encodes the stearoyl CoA desaturase, inSaccharomyces cerevisiae. We controlled the amount of UFA taken up by the cell by varying the concentration of tergitol in the medium. When cultured with 1 mM fatty acid in 0.1% tergitol, cells took up much more fatty acid than when cultured with the same concentration of fatty acid at 1% tergitol, although the amount incorporated was dependent on UFA species. For each fatty acid tested, we found that the higher uptake (0.1% tergitol condition) had a stronger impact onOLE1regulation. A principal product of the desaturase 16:1∆9, and the nonnative UFA 18:2∆9,12, most strongly repressed the reporter constructOLE1-lacZtranscription, while the other major product of the desaturase, 18:1∆9, and the nonnative UFA 17:1∆10 caused a more diminished response. Based on these results, our initial hypothesis was thatOLE1was regulated in response to membrane fluidity; however, subsequent work does not support that idea; we have found that conditions that affect membrane fluidity such as growth temperature and growth with saturated ortransfatty acid supplementation, do not regulateOLE1in the direction predicted by fluidity changes. We conclude that at least one signal that regulatesOLE1transcriptional expression is most likely based on the fatty acids themselves.
Highlights
In the yeast Saccharomyces cerevisiae, there is a single fatty acid desaturase encoded by the OLE1 gene [1, 2]. e stearoyl-CoA desaturase, which functions as a homodimer [3], introduces a cis double bond between carbons 9 and 10 of the acyl chain
Its primary products in vivo are palmitoleic (16:1∆9) (x:y∆n, fatty acids containing x carbon atoms and y cis double bonds located at position n from the carboxyl end; UFA, unsaturated fatty acid) and oleic acid (18:1∆9) [4]. ere is accumulating evidence that aberrant expression of the stearoyl-CoA desaturase is involved in disease; in mammals, an anticancer gene ORCTL3 was identified that could cause apoptosis in certain transformed cells [5]
Recent investigations have identified a role of ARV1 in fatty liver disease [8]. e yeast arv1 mutants are defective in OLE1 regulation, implying a possible connection between fatty liver disease and desaturase expression
Summary
In the yeast Saccharomyces cerevisiae, there is a single fatty acid desaturase encoded by the OLE1 gene [1, 2]. e stearoyl-CoA desaturase, which functions as a homodimer [3], introduces a cis double bond between carbons 9 and 10 of the acyl chain. OLE1 expression is regulated at the level of transcription, RNA stability and protein activity The UBX2 encoded protein has been shown to be important in the regulation of OLE1 in response to exogenous fatty acids, acting as a bridging factor between the cytosolic Cdc48p-Npl1p-Ufd1p complex with the membrane associated ubiquitin ligase complex and Mga2p and Spt23p [25, 26]. We examined conditions that alter membrane fluidity to try and detect a consistent molecular response
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