Science

The Secrets of Brewer's Yeast

The penicillin of fungal infection will be better, smarter, and more resilient.

Paul Rowley

Lovers of good food and drink everywhere will be surprised to learn that Saccharomyces cerevisiae — a species of yeast that allows for the delicious fermentation found in our favorite food groups of beer, bread, and wine — is chronically infected with viruses. Lots of them. In fact, even some research scientists who have spent their career studying this organism are oblivious to this fact, says Paul Rowley, yeast virus expert and assistant professor with the University of Idaho.

“In any one cell, you can have up to nine different types of viruses infecting the cell,” he tells Inverse.

It’s surprising, but there’s nothing to be worried about. Your beer is safe, and the yeast isn’t really sick. So few people pay attention to these viruses because under most conditions, they don’t do all that much. Unlike the viruses we’re more used to, they don’t reproduce inside a cell until it bursts and dies, allowing them to move on to new hosts. Instead, they spread through cell sex — when two haploid yeast cells come together as one. The viruses do well when their hosts do well, so characteristics that would hurt the host environment are not in their evolutionary They are the super common and almost completely benign STDs of the yeast world — like herpes if herpes didn’t occasionally erupt into itchy sores and deadly cancers.

Paul Rowley.

Here’s the twist: Under a very specific set of circumstances, the viruses go from benign to helpful, emitting toxins that are harmless to the infected host but deadly to some other yeasts and fungi, turning the host cell into a so-called “killer yeast.” By clearing out the competition, the virus helps itself — and therefore itself — to succeed.

It’s a bizarre phenomenon, and one that’s not yet completely understood by scientists. But if we could unlock the secrets of these killer yeast systems, it could change the world, says Rowley.

“We essentially ‘beat’ bacteria, really, for a short amount of time, with antibiotics; we’ve never beaten fungi, ever,” says Rowley “They’ve always been there, and they’ve always been pervasive in their attack of our crops and our livelihoods. Billions of dollars of crops are lost every single year due to either fungal infection pre-harvest, or spoilage post-harvest.”

Starting from the naturally occurring toxins produced by these killer yeast, it may be possible to develop the penicillin of the fungal world, only better. Rather than wiping out all types of fungus in an environment, these toxins could in theory be engineered to very specifically target the organism causing problems, while leaving microbes contributing to a healthy ecosystem unharmed.

Killer yeasts inhibit growth of nearby organisms by excreting toxins.

Imagine effective and targeted weapons against potato blight, which spread famine through Europe in the 19th century, or chestnut blight, which killed off the American chestnut tree to near extinction in the 20th century. These days, fungal disease has spread into the animal kingdom in a major way, threatening bees, bats, and amphibians in many parts of the world with their very existence. The consequences to ecosystems, food supplies, and human health that result from these losses are enormous.

The dream of smart fungicides targeted against these threats could be achieved in Rowley’s lifetime, he says. But first, scientists have to do the sort of basic experimentation that will lead to a better understanding of how killer yeasts work. The brilliant thing about these toxins is that they are protein-based, which means that all of the tricks of genetic engineering can be used to manipulate and adapt them — a serious advantage.

But there’s a long way to go. Here’s how narrow a set of circumstances are required to get a killer yeast to exhibit its killer characteristic. It takes a yeast that is infected with a certain virus, and then that virus must itself be infected with a certain satellite virus. It’s the satellite virus that produces the toxin, and without all of these pieces in order, you don’t have killer yeast.

In order to have killer yeast, you must also have a thing to be killed. A given toxin will only work on specific organisms — sometimes even within the same species only certain strains will be vulnerable to a given killer yeast system, and scientists aren’t yet sure why that is, or how to tell apart the sensitive strains from the invulnerable.

Now, if you have the right killer yeast, and the right target yeast, nothing will happen unless you have the right environmental conditions; the toxins only work within a narrow range of pH and temperature.

Killers yeasts painted onto a medium demonstrate their killer abilities.

But, if you get all of this right, the magic happens. Rowley demonstrates this to students and the world at large by covering a petri dish with a thin layer of the strain of yeast that is sensitive to the toxin. On top, he paints on the killer yeast strain in, say, the classic icosahedral shape of a viral capsid. As the culture develops, the killer yeasts should do well and inhibit growth in nearby areas. The medium is dyed with methylene blue, and concentrates in the regions of cell death, showing in a clear picture the signature of a killer.

“I love it,” says Rowley. “Often scientists don’t have the ability to really show, in nice graphics, what they do. It’s always gels and colorless liquids, and things like that. But this is actually a beautiful plate-based assay that we can be used to look at the interaction between the virus and the host.”

It’s fun science, but it could also one day lead to a revolution in how we manage agriculture and environments. In the future, we humans might even get over their obsession with sterilization and control, and opt instead to invite the microbial world in, armed with good tools against nasty intruders.

“Fungi and bacteria, they’re always going to find ways to become resistant; it’s just a fact,” says Rowley. “There are many ways that fungi can become resistant to these toxins. But the question is, if we understand what those mechanisms are, then we can combat them, too. We can be smart about how we do this.”

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