Let's Not Get Stressed
Can we be anti-oxidant about it?
Dear Brew Enthusiasts,
Please find below another instalment of The beerologist. It must be Friday!
In this weeks post, we will talk about the anti-oxidant capacity of yeast. In other words, how can make yeast more resistant to oxidation? Is there anything we can learn by studying the biology of yeast?
In a paper published this year, Jinjing Wang and authors (2021) investigated the activity of genes and pathways involved in anti-oxidant production in yeast. The (widely accepted) view that beer oxidation affects beer quality and freshness underpinned the main reasons for their study.
The key finding that helped drive this study forward was that a mutant yeast strain (named P-127) was outperforming regular lager strain in the production of anti-oxidants. The authors measured 1,1-diphenyl-2-picrylhydrazyl (DPPH) scavenging ratios, thiobarbituric acid (TBA) values, resistant staling value (RSV), and stability index (SI) for beers made with both P-127 and Pilsner yeasts. These analyses confirmed that the mutant significantly improved the anti-oxidant activity in beer.
This mutant, then enabled the authors to carry out transcriptome (gene expression) analyses and metabolome analyses (measuring the levels of yeast metabolites in yeast cells or beer) and identify differences that could underpin anti-oxidant activity. Using gene expression analyses, the authors identified 943 genes that were downregulated in P-127 when compared to Pilsner and 948 genes that were upregulated. These results suggest that the changes in anti-oxidant activity are due, to some extent, to changes in gene expression in the mutant strain.
The researchers then looked at metabolite fluxes and the differences between strains that could help explain their observations to investigate this further. Metabolite analyses identified 443 metabolites that were changing significantly between the two strains. I have summarised the results below.
The activity of the mannose synthesis and hexose transport pathways are altered in the mutant. Gene expression and metabolite analyses revealed that genes for mannose synthesis were elevated in the mutant and consistent with their results. These metabolite levels were higher in the mutant strain.
Gene expression also revealed differential expression of the members of the Hxt gene family, a group of genes thought to be involved in sugar transport. Available information describing their roles and their expression in these experiments suggest enhanced uptake of sugars (fructose and glucose) and export of mannitol (and possibly sorbitol) in the mutant.
Changes in oxidative phosphorylation pathway, the TCA cycle, pyruvate metabolism and amino acid metabolism
Respiration (conversion of sugar to energy) takes place in the mitochondria in a process that is controlled by a large number of respiratory proteins. Intriguingly, many of these genes were downregulated in the mutant, suggesting that the mutant has a lower metabolic rate. Possibly consistent with a lower respiratory rate, overall metabolism (TCA cycle, amino acid metabolism) also slowed down.
The authors suggest that these changes in metabolic and respiratory rates create an intracellular environment that is more resistant to oxidative stress (which is, in part, caused by respiration in the yeast mitochondria). By reducing the levels of active oxygen species and producing metabolites with anti-oxidant activity, the mutant yeast strain can better deal with oxidative stress.
Why is this important?
Oxidative stress is an important factor that helps determine yeast performance. With this study, the authors have identified the molecular pathways that could elevate resistance to oxidative stress and help yeast perform better during fermentation. One can envisage a strategy in which new yeast strains, metabolically adapted to oxidative conditions, are engineered to help brew better beer.
I hope you enjoyed this read. Have a great weekend!
Edgar, The Beerologist