In Saccharomyces cerevisiae ΔRIB1 and ΔRIB4 mutants, riboflavin auxotrophy is reverted by Wolbachia (wStr) infection.

In endosymbiosis, unicellular organisms, mostly prokaryotes, live inside the cells of a host that may be uni- or multicellular. More than half insect and arthropod species host the obligate endosymbiont Wolbachia spp., an alpha-proteobacterium that, given time, may coevolve with its host and progress from parasitism to strict mutualism, where an obligate endosymbiont avoids rejection by providing advantages to the host such as essential nutrients. It was recently found that in the wild yeasts may host both facultative and obligate endosymbionts. To model host-symbiont mutualist interactions in yeast, we tested two different Saccharomyces cerevisiae riboflavin-synthesis pathway deletion mutants (ΔRIB1 and ΔRIB4), finding that these failed to grow in the absence of exogenous riboflavin (RF), i.e., they were RF-auxotrophic strains. In both mutants Wolbachia infection cured auxotrophy. In addition, Wolbachia infection led to a mild increase in survival to exposure to 1 M NaCl or to 10 mM hydrogen peroxide. The artificial yeast/endosymbiont model proposed here may become a useful tool to explore parasitic, facultative and mutualist associations.