In a recent study, scientists learn the genetic basis for different wine varieties.
Since the beginning of recorded history, humans have had a fascination with intoxicants – particularly, ethyl alcohol. This is evidenced by the myriad ways we produce and consume this substance: beer, wine, and spirits, each of which has countless styles, flavors, origins, and culture. Consequently, we have put large-scale efforts (and dollars) into researching and developing every aspect of alcohol production, from crop choice to drinking techniques.
Pinot is an ancient grapevine variety and is the origin of the Pinot vine types that we recognize today on our wine bottle labels, such as Pinot noir, Pinot blanc, and Pinot gris. However, the emergent diversity of the Pinot variety is no run-of-the-mill evolutionary story. To ensure a consistent end product, Pinot vines used in winemaking are usually grown by propagating or grafting, whereby plants do not grow to maturity from seed, but rather directly from a cutting of an original vine. Notably, this practice means the vines are clones of one another. So how do we have several varieties of Pinot, all of which produce different types of wines, when we have simply been cloning a single, original variety?
Last week, scientists led by Frédérique Pelsy at INRA Colmar, France, explained the answer to this question in work published in the online journal PLOS Genetics. The research describes an interesting consequence of human intervention in the evolution of a family of winemaking grapevines called Pinot.
Unlike in our beloved science fiction genre, clones in nature are not created equal. The team studied 33 diverse clones (talk about two words that shouldn’t go together) of Pinot noir, Pinot blanc, and Pinot gris. These plants are nearly morphologically identical except for the color of their fruit. For the first time, the mechanisms behind clonal genetic differences in the Pinot family have been described.
During the process of growth and development, the cellular machinery that replicates DNA often makes mistakes. This cellular level error is called “somatic mutation”, and is the cause of diseases such as cancer in the human body. Somatic mutations are not heritable because they occur in cell types that do not get passed on to offspring. The mutations typically arise because of sheer probability: the molecules that replicate DNA rarely make mistakes, but when you are talking about billions of cells replicating over hundreds of generations during an organism’s lifespan, rarely turns out not to be a trivially small number.
Back to the story at hand: The authors studied a stretch of DNA in these Pinot grapevines that includes the gene that produces the color pigment anthocyanin, the molecule that gives the grapes their distinctive color. They found evidence for large-scale deletions and gene exchange in the different varieties (noir, gris, blanc) that resulted in somatic mutations. These mutations cause the loss of one or both of the copies of the fruit color gene, leading to the different appearance of these varieties.
The most meaningful conclusion, though, has to do with the type of mutations that occur. Since somatic mutations arise from a mistake in one, or very few, cells, they only affect a small part of the plant. However, through the many hundreds or thousands of generations of clones and rounds of artificial selection, these small-scale mutations began to manifest themselves in the fruit appearance and could be noticed and selected by humans.
These seemingly insignificant and rare somatic mutations, driven by the cloning of grapevines (rather than natural sexual reproduction) and the desire to make consistent tasting wine, produced the three varieties of Pinot that are widely used around the world today. It is amazing that we are able to derive this information from applying what we know about molecular genetics to subtle genetic signatures. Similar work has been done in other fields such as the history of animal domestication, and will surely continue to uncover the fascinating history of human-caused evolution.