TAILIEUCHUNG - Báo cáo khoa học: Mutants of Saccharomyces cerevisiae deficient in acyl-CoA synthetases secrete fatty acids due to interrupted fatty acid recycling

In the present study, acyl-CoA synthetase mutants of Saccharomyces cerevisiae were employed to investigate the impact of this activity on cer-tain pools of fatty acids. We identified a genotype responsible for the secre-tion of free fatty acids into the culture medium. | ỊFEBS Journal Mutants of Saccharomyces cerevisiae deficient in acyl-CoA synthetases secrete fatty acids due to interrupted fatty acid recycling Michael Scharnewski1 Paweena Pongdontri1 Gabriel Mora1 Michael Hoppert2 and Martin Fulda1 1 Department of Plant Biochemistry Albrecht-von-Haller Institute Georg-August University Goettingen Germany 2 Institute for Microbiology and Genetics Georg-August University Goettingen Germany Keywords endoplasmic reticulum FAA FAT1 fatty acid accumulation lipid remodelling Correspondence M. Fulda Department of Plant Biochemistry Albrecht-von-Haller Institute for Plant Sciences Georg-August University Goettingen Justus-von-Liebig-Weg 11 D-37077 Goettingen Germany Fax 49 551 39 5749 Tel 49 551 39 5750 E-mail mfulda@ Present address Department of Biochemistry Faculty of Science Khon Kaen University Thailand Received 9 January 2008 revised 12 March 2008 accepted 20 March 2008 In the present study acyl-CoA synthetase mutants of Saccharomyces cerevisiae were employed to investigate the impact of this activity on certain pools of fatty acids. We identified a genotype responsible for the secretion of free fatty acids into the culture medium. The combined deletion of Faa1p and Faa4p encoding two out of five acyl-CoA synthetases was necessary and sufficient to establish mutant cells that secreted fatty acids in a growth-phase dependent manner. The mutants accomplished fatty acid export during exponential growth-phase followed by fatty acid re-import into the cells during the stationary phase. The data presented suggest that the secretion is driven by an active component. The fatty acid re-import resulted in a severely altered ultrastructure of the mutant cells. Additional strains deficient of any cellular acyl-CoA synthetase activity revealed an almost identical phenotype thereby proving transfer of fatty acids across the plasma membrane independent of their activation with CoA. Further experiments identified membrane lipids as the .

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