It's not just fluff: mechanisms underlying the ability of Saccharomyces cerevisiae to build complex multicellular colonies

Abstract

Most colonies formed by <italic>S.cerevisiae</italic> are simple domes, not surprising considering the yeast is a unicellular organism. However, certain <italic>S.cerevisiae</italic> strains are able to form complex and intricately patterned colonies that involve the formation of multicellular structures. The colony patterns formed by these strains are highly reproducible, indicating that they result from a well defined developmental path. Understanding this remarkable ability could give us insights into important biological phenomena such as biofilm formation, biological shape and pattern determination and the genetic architecture underlying complex traits. In this dissertation, the efforts taken to uncover the molecular mechanisms through which <italic>S.cerevisiae</italic> is able to achieve the formation of complex colony morphology are described. Through the thorough characterization of a novel switching phenomenon, we discover that the gain and loss of a single chromosome allows <italic>S.cerevisiae</italic> a quick, heritable and stable mechanism through which they are able to toggle their ability to form these complex colonies. This switch is made all the more remarkable with the realization that the phenotypic state of the colonies is able to confer fitness advantages in different conditions. The finding that the increased dosage of a single gene is sufficient for this switch then fuels an overexpression screen that uncovers novel suppressors of the trait. Through the further characterization of the transcriptome of several fluffy and smooth strains, we discover the importance of extracellular proteins for the formation of these colonies and how their expression is correlated with their molecular function. In summary, the findings described here not only newly implicate several proteins in the modulation of the trait and highlight the distinct transcriptional regulation of the mechanistic effectors of the trait, but also provide further insight into how aneuploidy is able to modulate the phenotypic state and fitness of an organism.