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A more recent version of this article appeared on August 1, 2002
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Submitted on February 7, 2002
Revised on May 27, 2002
Accepted on June 5, 2002
1 Laboratory of Biochemistry, Academic Medical Center, Meibergdreef 15, 1105 AZ Amsterdam, Swammerdam Institute for Life Sciences, Nieuwe Achtergracht 166, 1018 WV, University of Amsterdam, The Netherlands
2 Laboratory of Biochemistry, Academic Medical Center, Meibergdreef 15, 1105 AZ Amsterdam, Swammerdam Institute for Life Sciences, Plant Pathology, Nieuwe Achtergracht 166, 1018 WV, University of Amsterdam, The Netherlands
3 Laboratory of Biochemistry, Academic Medical Center, Meibergdreef 15, 1105 AZ Amsterdam, Swammerdam Institute for Life Sciences, Plant Pathology, Nieuwe Achtergracht 166, 1018 WV, University of Amsterdam, The Netherlands (present address: Department of Biological Sciences, Columbia University, 1212 Amsterdam Avenue, MC 2441, New York, NY 10027, USA)
4 Laboratory of Biochemistry, Academic Medical Center, Meibergdreef 15, 1105 AZ Amsterdam, Swammerdam Institute for Life Sciences, Microbiology, Nieuwe Achtergracht 166, 1018 WV, University of Amsterdam, The Netherlands
5 Laboratory of Biochemstry, Academic Medical Center, University of Amsterdam, Meibergdreef 15, 1105 AZ Amsterdam, The Netherlands
* Corresponding author. E-mail address: H.F.Tabak{at}AMC.UVA.NL.
Yeast cells were grown in glucose-limited chemostat cultures and forced to switch to a new carbon source, the fatty acid oleate. Alterations in gene expression were monitored using DNA micro-arrays combined with bioinformatics tools, among which the recently developed algorithm REDUCE. Immediately after the switch to oleate, a transient and very specific stress response was observed, followed by the upregulation of genes encoding peroxisomal enzymes required for fatty-acid metabolism. The stress response included upregulation of genes coding for enzymes to keep thioredoxin and glutathione reduced, as well as enzymes required for the detoxification of reactive oxygen species (ROS). Among the genes coding for various iso-enzymes involved in these processes only a specific subset was expressed. Not the general stress transcription factors Msn2 and Msn4, but rather the specific factor Yap1p appeared to be the main regulator of the stress response. We ascribe the initiation of the oxidative stress response to a combination of poor redox flux and fatty acid-induced uncoupling of the respiratory chain during the metabolic reprogramming phase.
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