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A Saccharomyces cerevisiae pgs1 null mutant, which(CL) biosynthesis, grows well on most fermentable carbonsources, but fails to grow on non-fermentable carbon sourcessuch as glycerol, ethanol, and lactate. This mutant also cannotgrow on galactose medium as the sole carbon source. Wefound that the incorporation of [14C]-galactose, which is thefirst step of the galactose metabolic pathway (Leloir pathway),into the pgs1 null mutant cell was extremely repressed.Exogenously expressed PGS1 (YCpPGS1) under indigenouspromoter could completely restore the pgs1 growth defect onnon-fermentable carbon sources, and dramatically recovered[14C]-galactose incorporation into the pgs1 mutant cell. However,PGS1 expresion under the GAL1 promoter (YEpPGAL1-PGS1-myc) could not complement pgs1 null mutation, and the GAL2-lacZ fusion gene (YEpPGAL2-lacZ) also did not exhibit its β-galactosidase activity in the pgs1 mutant. In wild-type yeast,antimycin A (1g/ml), which inhibits mitochondrial complexI, severely repressed not only the expression of the GAL2-lacZ fusion gene, but also uptake of [14C]-galactose. However,exogenously expressed PGS1 partially relieved these inhibitoryeffects of antimycin A in both the pgs1 mutant and wild-typeyeast, although it could not basically restore the growth defecton galactose by antimycin A. These results suggest that thePGS1 gene product has an important role in utilization ofgalactose by Gal genes, and that intact mitochondrial functionwith PGS1 should be required for galactose incorporation intoPGS1 gene might provide a clue toresolve the historic issue about the incapability of galactosewith deteriorated mitochondrial function.

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