[P003] Poster

12:10 PM - 1:00 PM JST(3:10 AM - 4:00 AM UTC)

[P02-159] The Relationship Between Purine Compounds in Beer and Yeast Nucleotide Metabolism

○Yusuke Oizumi¹, Yoko Yasuda¹, Toshiko Kutsukake¹, Taku Ota¹, Kentaro Iwasaki¹ (1. Institute for Future Beverages, Kirin Holdings Company, Limited (Japan))

Keywords:

Purine compounds,Beer,Fermentation process,Saccharomyces pastorianus,Nucleic acid synthesis pathway,Xanthine,Adenine-requiring strains

Purines are a collective term for substances with a purine structure, including purine bases, purine nucleosides, purine nucleotides such as ATP, and nucleic acids. Generally, the purines ingested by humans are broken down into uric acid and excreted from the body. However, when the amount of uric acid exceeds the excretory capacity and accumulates in the body, it causes hyperuricemia and gout. Therefore, there is a demand for the development of foods and beverages with low purine content.Purine compounds in beer, such as adenine, guanine, hypoxanthine, and xanthine, show different behaviors throughout fermentation. While adenine, guanine, and hypoxanthine decrease, xanthine increases during fermentation phase. The synthesis of xanthine is believed to be significantly influenced by intracellular nucleic acid synthesis pathways. Meanwhile, in sake production, strains with natural mutations in the nucleic acid synthesis pathway, specifically adenine-requiring strains, are commonly used for brewing pink cloudy sake.
In this study, we conducted wort fermentation tests using adenine-requiring yeast strains. Our findings revealed that the use of these strains resulted in reduced xanthine production. Metabolite analysis using CE-TOFMS showed that adenine-requiring strains accumulated FGAM, an intermediate metabolite in the nucleic acid synthesis pathway, without accumulation of the downstream metabolite AIR. Further genetic analysis identified mutations in the ADE5,7 gene, which encodes the enzyme responsible for converting FGAM to AIR in the nucleic acid synthesis pathway. Further analysis using AlphaFold2 indicated that the mutation was located in the dimerization domain of Ade5,7 protein, suggesting that the inability to form dimers could have inhibited AIR synthesis.These findings suggest that the lower xanthine production in adenine-requiring strains is partly caused by the defect in the Ade5,7 enzyme.