CHENG Yu-rong, SUN Zhi-jie, CUI Qiu. Research of a specific competitive inhibitor of pyruvate dehydrogenase complex on Aurantiochytrium synthesizing fatty acids[J]. Science and Technology of Food Industry, 2016, (16): 161-166. DOI: 10.13386/j.issn1002-0306.2016.16.024
Citation: CHENG Yu-rong, SUN Zhi-jie, CUI Qiu. Research of a specific competitive inhibitor of pyruvate dehydrogenase complex on Aurantiochytrium synthesizing fatty acids[J]. Science and Technology of Food Industry, 2016, (16): 161-166. DOI: 10.13386/j.issn1002-0306.2016.16.024

Research of a specific competitive inhibitor of pyruvate dehydrogenase complex on Aurantiochytrium synthesizing fatty acids

  • Aurantiochytrium synthesizes polyunsaturated fatty acid( docosahexenoic acid( DHA) and docosapentaenoic acid( DPA)) through polyketide synthase( PKS) pathway,and saturated fatty acid( mainly palmic acid and oleic acid) through fatty acid synthase( FAS) pathway.Both pathways competitively used acetylCo A as carbon precursor. Understanding the mechanism to regulate the carbon partition between FAS pathway and PKS pathway was helpful for designation of high- DHA- yield strains and optimization of industrial fermentation process.In this research,the pyruvate dehydrogenase complex,which catalyzing the synthesis of acetyl- Co A,was treated by fluoropyruvate( FP)- a specific substrate- competitive inhibitor. Based on determination of carbon consumption,biomass,total oil accumulation and the distribution ratio of acetyl- Co A between FAS and PKS pathways were investigated.The results showed that FP could be assimilated and metabolized by Aurantiochytrium and FP could inhibit lipid synthesis and significantly change the partition ratioof acetyl- Co A between FAS and PKS pathways.Production of carbon- dioxide was enhanced by FP,but the accumulation of biomass was inhibited.These results hinted that the affinity of FAS pathway to acetyl- Co A was higher than that of PKS pathway and the content of polyunsaturated fatty acid( DHA and DPA) in total oil could not be increased by reducing supply of acetyl- Co A.
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