Alan Bakalinsky

Associate Professor, Food Science and Technology
Affiliate Faculty, Microbiology

CONTACT INFORMATION:
Office:Wiegand 216
Email:alan.bakalinsky@oregonstate.edu
Phone:(541) 737-6510
Links: Departmental Web Page
Pub Med

EDUCATION:
Ph.D. 1989, University of California, Davis

KEYWORDS: Yeast Genetics; Saccharomyces cerevisiae; Stress; Toxicity; Wine; Fermentation
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RESEARCH:
Winemaking is stressful business and not just for the winemaker and grape grower. These two individuals are joined by a third character — the wine yeast Saccharomyces cerevisiae — whose indispensable role in the process was only recognized about 150 years ago. Stated differently, if humans have been making wine for the last 7,000 years as suggested by archeological evidence, and we imagine these years to span a single 24-hour day, yeast's essential role would have been discovered only in the last half hour of that day! And what of the stresses of the fermentation? While this species is probably the most alcohol-tolerant organism on the planet, life during fermentation is no picnic, and in the end, accumulation of ethanol-induced damage is the most likely cause of death. This organism's love affair with sugar exposes it to great osmotic pressure as sugar concentrations in ripe grapes can easily exceed 25%. The ancient practice of adding sulfite to the fermentation as an antioxidant and mild antimicrobial agent to protect against contaminating microbes is yet another stress that yeast has learned to overcome. A successful history of adapting to environmental headaches — some a product of human domestication — combined with a wealth of available biochemical, molecular, and genomic information unmatched in any other eukaryote, has made S. cerevisiae a powerful model for discovering mechanisms that underlie the physiology of adaptation. Because essential functions are broadly shared among distantly-related species, what is true in this organism is very likely to be relevant to humans and other higher eukaryotes as well. My laboratory uses this model species to learn how cells respond to various environmental hazards. We also have a keen interest in understanding the specific contributions of this organism to wine quality.

Current projects:
Contributions of yeast mannoproteins to wine quality. Grape tannins contribute color, bitterness, and astringency to wine. Winemakers modify the amounts and quality of tannins in red wines by controlling extraction, post-fermentation oxygenation, addition of fining agents and wood extracts, and aging practices. We hypothesize that aging red wine on the yeast lees (yeast biomass generated during fermentation) results in a desirable reduction in astringency due to formation of complexes between grape tannins and yeast-derived mannoproteins. We are interested in documenting this possibility by detecting, identifying, and monitoring the kinetics of release of yeast mannoproteins during aging of red wine on the yeast lees.

Oxalate-mediated plant disease. Oxalic acid occurs widely in nature and is a recognized virulence factor produced by several phytopathogenic fungi, including Sclerotinia sclerotiorum, the causal agent of white mold and related diseases. As such, oxalate likely mediates host cell wall degradation and plant disease symptoms by chelating pectin-bound calcium, by lowering the pH of infected plant tissue to a level more optimal for fungal cell wall-degrading enzymes, by suppressing the defense-related oxidative burst, and by inducing stomatal opening. While oxalate does not appear to be a normal metabolite in S. cerevisiae, the molecular targets for oxalic acid-mediated toxicity in this species may still be shared among plants and their oxalate-secreting fungal pathogens. We recently screened a S. cerevisiae deletion library for mutants sensitive to oxalic acid in order to discover oxalate-protective genes whose orthologs may encode protective functions in plants and in oxalate-secreting phytopathogenic fungi. We are currently following up on the observations that the most oxalate-sensitive yeast mutants are impaired in vesicle-mediated transport or are defective in riboflavin uptake.

Nanomaterial toxicity. The nanotechnology industry is growing at a rapid pace due to the multitude of applications for engineered nanomaterials. At the same time, environmental and human exposure to these materials is expected to increase proportionally. While fullerenes and derived materials have been demonstrated to possess antioxidant activity in vivo and in vitro, they have also been reported to induce oxidative stress, growth inhibition, inflammation, and other undesirable health effects. At a mechanistic level, it is not obvious how to reconcile these contradictory observations. We are interested in determining the mechanisms by which manufactured nanomaterials cause cytotoxicity in realistic environments of exposure and are currently using a genomics approach to identify genes and functions that are protective against toxicity caused by fullerene and fullerol in the yeast model.