Sometimes yeast gets convinced to enter into an unusual partnership

by Matthias Eder .

Ever since the movie “Finding Nemo” the image has been fixed in the mind of the audience: The orange and white striped clownfish which is inseparably connected to its anemone and never moves too far away from it. This unusual partnership has advantages for both sides – since fish and anemone are each protected from their predators. The clownfish however is not resistant to the stinging cells of the anemone from the beginning, this protection is only transferred to it from the anemone after their first contacts.

In nature, there are many examples of symbiotic partnerships where the actors not only mutually benefit from each other, but also influence each other specifically. But why should a principle that works on a large scale not also work on a small scale? Last year a group of scientists led by Daniel F. Jarosz from Stanford University and MIT discovered exactly this when they stumbled over the unusual relation between yeasts and bacteria.

The principle of this partnership is based on a conserved biological circuit, called catabolite repression, that prevents yeast from utilizing other carbon sources when glucose is present. In fact, several organisms have such mechanisms. However it is particularly pronounced in the baker’s yeast Saccharomyces cerevisiae and has probably led to the case that man started to use this yeast to produce alcohol.

The scientists had plated baker’s yeast on nutrient medium which contained glycerin and a small amount of glucosamine. Glucosamine cannot be utilized by the yeast, but activates the catabolite repression due to its structural similarity to glucose. The yeast was therefore also not able to make use of the available glycerol. However, an inadvertent bacterial contamination of Staphylococcus hominis allowed the yeast cells close to the bacteria colony to consume glycerol and grow, despite the present glucosamine. This ability was also retained when the cells were transferred to new medium without the neighboring bacteria. It was even transmitted to the following generations. The yeast was thus subjected to a heritable change.

The group around Daniel F. Jarosz had found out in previous studies that the catabolite repression of yeast can be suppressed by [GAR+], a prion-based epigenetic element. Prions are proteins which exist in different conformations and which are able to induce a conformal change in other proteins of their kind. The scientists tested the yeasts which had come in contact with the bacteria on [GAR+] and were able to detect the prion, whereas other prions remained unaffected. The researchers set out to show the mechanism by which the bacteria caused the conformational change. Bacterial extract could be boiled, frozen, treated with enzymes and be filtered through a 3 kDa filter, it always retained its [GAR+] inducing properties. The molecule(s) that influence [GAR+] must therefore be small and stable, but still more work needs to be done in order to identify them.

Interestingly, the ability to induce [GAR+] could also be detected for other bacteria, which were not necessarily closely related to each other. This communication is broadly conserved, providing an argument for its adaptive value and thus making it an unique example of Lamarckian inheritance.

But which mutual benefits do yeast and bacteria have from their partnership? The advantage for the yeast is obvious. It becomes able to access a greater variety of carbon sources, which has a positive effect on its growth and viability. The advantage for the bacteria cannot be seen at once. However yeasts produce smaller amounts of alcohol when they feed on carbon sources other than glucose. This is beneficial for the bacteria as higher concentrations of alcohol are toxic for them.

It is just as with the clownfish: Sometimes you have it easier in life when you can rely on the benefits of a partnership.

 

References

Jarosz DF, et al. (2014)  Cross-kingdom chemical communication drives a heritable, mutually beneficial prion-based transformation of metabolism. Cell 158(5):1083-93.

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