Indigenous yeast in Sauternes, multi-species family wineries, and Casale’s Trebbiano orange wine

A group of French scientists, mostly based in Bordeaux, have recently published evidence* that the same Saccharomyces cerevisiae populations have lived at their winemaking homes in Sauternes for at least 23 years.** Two decades is a brief moment, whether you’re measuring in human-history-of-Sauternes time or in yeast-evolution time, but their work still supports the idea that yeast populations become associated with wineries and stick to them.

A main point the scientists aim to make is that these longstanding, tradition-following Sauternes estates haven’t been badly polluted by modern, commercial winemaking yeasts. Only seven percent of the S. cerevisiae strains they collected could be clearly connected to specific commercially produced strains. This news is excellent for those in the natural wine camp who want to call spontaneous ferments “natural” or “wild.” In this little corner of Sauternes, at least, it seems that wines allowed to ferment spontaneously aren’t just being fermented by commercial yeasts persistent in the environment. Most of the work of fermentation is indeed being done by yeasts which very likely existed in the area prior to Lallemand and the rest introducing their tidy little foil packets of active dried specimens.

A good case can be made, I’d argue, for calling those non-commercial yeast something like “domesticated indigenous” rather than “wild:” human winemakers have selected and bred them up for desirable winemaking characteristics over many generations, just as human dog-keepers have bred up select canine features or orchid aficionados have carefully developed new plants. Domestication can happen even if living things are never bought and sold.

Regardless of what we choose to call these yeast species, though, this sort of research says that those species are part of the traditional winemaking environment, part of the terroir. Terroir is apt because that complex term incorporates human traditions and activities, the way winemakers and the rest of the community have shaped the land and its various characteristics: soil, plant life, microbial life, architecture, machinery, maybe some canines. Terroir doesn’t force us to make a choice between those winery-associated yeasts being wild or cultivated. They’re both, and winemakers and winemaking have evolved with them.

The Casale orange trebbiano*** I opened last night is made by a winery with whose winemaking history in their neck of Chianti can be traced back to 1770. The wine itself is a 2012 vintage and the current release, kept on the skins for 30 days and in stainless steel for two years. The property is biodynamic, the wine spontaneously fermented.

Even if the mid-palate is fairly empty, the nose and the finish are more than enough to rescue that deficiency: savory, nutty, sweetly orange blossomy and honeyed up front all at once, and acidity with great energy and tension (minerality, if you wish) on the tail, with a pleasant light astrigency across the breadth of the middle. This isn’t just a wine for thinking with, and I’d readily pour it for anyone who thinks that all biodynamic orange wines must smell like hair salons and taste like dirt, because it doesn’t. But it’s a beautiful example of a wine good both for drinking and for thinking, that tastes pleasant and nourishing and that provokes pleasant and nourishing trains of thought.

When we care about family wineries – for the purely aesthetic value of tradition as well as the economic value of maintaining local businesses and the winemaking value of passing down knowledge and physical infrastructure – we should care about the extended family, not just the humans but the yeast (and maybe even other species) who have also lived on a winemaking property for generations, who make the wine with their human coworkers. Taking care of the family can’t be just about loving your brothers, or even about supporting the other families who might work with you, but about caring for your non-human brothers and coworkers. Now, that’s a pleasant and nourishing train of thought.

*Full text of the article behind an academic journal’s paywall, unfortunately.

**A bit more detail on that point: the team collected samples from three Sauternes estates over 2012, 2013, and 2014, isolating 653 individual yeast strains, and compared them to commercial strains and to 102 “library” isolates collected from one of the three estates between 4 and 23 years ago. The comparisons to determine which strains are related to which other strains rely on 15 “microsatellites,” or specific, small sections of DNA the sequence of which is highly and characteristically variable amongst strains. Much could be said about how we define what constitutes an individual “strain” on the basis of the tools we have available to do so – appearance (phenotype, in biology jargon) in the past, genetic today – but I’ll forgo that conversation for today.

***Purchased for £15.50 from Wood Winters in Edinburgh.

Endings and beginnings

Endings: of my PhD, of my research project on wine-industry science communication, of my time in New Zealand.

Beginnings: of a research fellow position at the University of Edinburgh, of new work on human-yeast interactions in synthetic biology, of my time in Scotland.

I’m no longer a few hours away from the fine wine-growing regions of Central Otago, Canterbury, and Marlborough. On the other hand, I’m a few hours (by air, at least) from the fine wine-growing regions across Europe and the southern UK, and a few steps away from wine purveyors with selections the likes of which I haven’t seen in years. I consider this a fair trade. The difference might even make up for not having a superb beach just outside my front door, though maybe I’ll withhold judgment on that one.

If you’re interested in synthetic biology, human-yeast collaboration and co-evolution, or if you’re in the UK and would like to strike up a conversation about other vinous or yeasty topics, feel free to contact me at erika(dot)szymanski(at)ed.ac.uk.

Effects of grapevine leafroll disease on wine quality (and when is a disease a disease?)

Gut reaction: Viruses cause disease. Disease is bad. Viruses are bad.

Gut reaction muted by a lot of recent genetics research: Viral DNA seems to be embedded in genomes all over the place. We’re not sure why a lot of it is there, or stayed there, or what it does while its there. Some viruses cause disease. Some don’t. Viruses are complex, and we probably don’t know the half of it yet.

A name like “grapevine leafroll-associated virus” gets you thinking about negative consequences. Rolled leaves don’t collect light efficiently, which means that they won’t contribute to the plant’s photosynthetic metabolism efficiently, which means that the plant may be malnourished, grow slowly, and/or not have enough energy to ripen fruit. Rolled leaves are bad. A virus that’s associated with rolled leaves is bad. But the virus is only associated, not causative. Some viruses in this general family of leafroll-associatedness aren’t associated with vine symptoms. And infected vines only show symptoms post-veraison (the stage of ripening at which grapes change color), even though they carry the virus in detectable quantities year-round.

Ergo, a group of vine and wine scientists headquartered in eastern Washington state designed an experiment to ask (published in PLOSOne, and therefore open-access to everyone): do grapes from vines with grapevine leafroll disease, and carrying one of these viruses (GLRaV-3), lag behind their undiseased counterparts throughout ripening, or only when vines show symptoms? Being particularly conscientious*, they also improved on existing studies of grapevine leafroll disease by collecting data for three consecutive years from a commercial vineyard, sampling grapes throughout the season but also harvesting grapes at the typical time and making wine from diseased and undiseased pairs, and subjecting those wines to (limited) chemical and sensory analysis. They also used own-rooted rather than grafted vines, which eliminates some potentially confounding variables.

Their conclusions, after collecting data over the 2009, 2010, and 2011 growing seasons:

  • Grapevine leafroll disease decreases vigor (as measured by cane pruning weights) and fruit yield in own-rooted Merlot vines in Western Washington.
  • Grapes from diseased/infected vines have lower total soluble solids (TSS) and higher titratable acidities (TA) (and, to a less dramatic degree, lower anthocyanin concentrations) than grapes from undiseased/uninfected vines, but only after vines begin displaying symptoms post-veraison.
  • Wines made from diseased grapes were browner and less intensely colored, earthier and less fruity, and more astringent compared with their undiseased counterparts.
  • However, panelists only correctly distinguished diseased from undiseased wines when served side-by-side in black glasses, removing the notable color differences from consideration and forcing them to differentiate on smell and taste alone.
  • Soluble solids, TA, and pH were all more dramatically affected than anthocyanins in diseased vines, which reflects the decoupling of anthocyanin development and sugar accumulation that happens late in ripening during which environmental conditions play heavy in anthocyanin development.

These conclusions probably do more for plant scientists than for commercial growers: data from one Merlot vineyard near Prosser can’t be precisely extrapolated to you, wherever you are, and thresholds for usable fruit are always a matter of context (the authors note that future studies should document the effects of grapevine leafroll disease on specific sensorily-important compounds). The study does add data points to a collection of statistically robust data that might help large companies make judgments about what they can include in their generic red blends before pH or some other parameter becomes a problem. But maybe the most interesting line of thinking here has to do with the nature of disease, and of relationships between viruses and diseases and symptoms. Do vines have leafroll disease before they exhibit symptoms? Where do we want to draw lines between normal or acceptable variation and disease symptoms? If a vine looks sad but makes grapes that make wine indistinguishable from happy-vine wine, and if genetic testing says that the plant also happens to have a virus, does that mean that the vine has a disease, or is it healthy?

Disease” can mean something different to the plant pathologist who looks at a vine, a geneticist who looks at the DNA of a vine, a commercial grower who looks at the fruit of the vine or a winemaker who looks at the juice it makes. That vine may be infected with viruses. Is the virus bad?

 

*Full disclosure: I know and think highly of several of the scientists on this team.