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Identification of novel genes for arachidonic acid metabolism in Saccharomyces cerevisiae (605.11)
Author(s) -
Batugedara Hashini,
Chikhalya Aniska,
HaasStapleton Eric
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.605.11
Subject(s) - saccharomyces cerevisiae , arachidonic acid , gene , biochemistry , fatty acid metabolism , transcriptome , yeast , biology , downregulation and upregulation , peroxisome , gene expression , enzyme
Saccharomyces cerevisiae produces prostaglandin E2 (PGE2) in the presence of arachidonic acid (AA). S. cerevisiae and its metabolites may be consumed in products manufactured using the yeast (e.g. beer) and yeast PGE2 can potentially modify human immune cell functions to exacerbate pre‐existing inflammation. The biochemical pathway utilized by S. cerevisiae to produce PGE2 is unknown. The identification of genes involved in AA metabolism may direct approaches to reduce off‐target effects of yeast PGE2 on immune cells. As S. cerevisiae does not have genes homologous to those involved in mammalian AA metabolism, identification of such genes will reveal a novel pathway for lipid biosynthesis. RNAseq transcriptome sequencing was conducted and we observed 2044 genes upregulated in yeast cultured with AA relative to the control yeast cultured without AA. Notably, genes encoding mitochondrial proteins that direct fatty acid beta‐oxidation (CRC1, YAT1 and CEM1) were upregulated 1.1‐3.0‐fold and genes encoding peroxisomal proteins that mediate beta‐oxidation of fatty acids (POT1, POX1, FAA1 and FAA2) were upregulated 1‐2.3‐fold. Upregulation of fatty acid metabolizing genes points to enzymes that may metabolize AA to produce PGE2 in S. cerevisiae. Currently, we are testing knock‐out strains of S. cerevisiae that lack the genes identified in the RNA‐seq studies for reduced PGE2 production. Grant Funding Source : Supported by a grant from the National Institutes of Health to E.J.H‐S (SC3GM092298).