Role of distinct dimorphic transitions in territory colonizing and formation of yeast colony architecture.

Microbial populations in nature often form organized multicellular structures (biofilms, colonies) occupying different surfaces including host tissues and medical devices. How yeast cells within such populations cooperate and how their dimorphic switch to filamentous growth is regulated are therefore important questions. Studying population development, we discovered that Saccharomyces cerevisiae microcolonies early after their origination from one cell successfully occupy the territory via dimorphic transition, which is induced by ammonia and other volatile amines independently on cell ploidy and nutrients.

The morphology of Saccharomyces cerevisiae colonies is affected by cell adhesion and the budding pattern.

Formation of organized colony morphology is clearly a result of organized, coordinated behavior of cells within a colony, which reflects changes in the cell environment, nutrient availability, inter- and intracolony signaling and others. Under standard conditions, colony morphology is specific to the particular yeast strain, which indicates that reproducibility of the structure appears to be a hallmark of programmed development. Our data indicate that markedly structured morphology of colonies formed by some haploid and diploid Saccharomyces cerevisiae strains is linked to formation of clusters of incompletely separated yeast cells organized into larger aggregates.

Different action of killer toxins K1 and K2 on the plasma membrane and the cell wall of Saccharomyces cerevisiae.

Study of Saccharomyces cerevisiae killer toxin-sensitive strains with the deltakre2 phenotype (resistant to toxin K1, sensitive to toxin K2) showed that the phenotype is complemented by the KRE2 gene not only in intact cells but also in spheroplasts, and resistance to K1 thus resides very probably in the plasma membrane. deltakre1 deletant displays a faulty interaction with both K1 and K2 toxin. Hence, Kre1p probably serves as plasma membrane receptor for both toxins.

Isolation and characterization of Saccharomyces cerevisiae mutants with a different degree of resistance to killer toxins K1 and K2.

Killer toxin K1 of Saccharomyces cerevisiae kills sensitive cells of the same species by disturbing the ion gradient across the plasma membrane after binding to the receptor at cell wall beta-1,6-glucan. Killer protein K2 is assumed to act by a similar mechanism. To identify the putative plasma membrane receptors for both toxins we mutagenized three sensitive S.

Domestication of wild Saccharomyces cerevisiae is accompanied by changes in gene expression and colony morphology.

Although colonies from Saccharomyces cerevisiae laboratory strains are smooth, those isolated from nature exhibit a structured fluffy pattern. Environmental scanning electron microscopy shows that the cells within wild fluffy colonies are connected by extracellular matrix (ECM) material. This material contains a protein of about 200 kDa unrelated to the flocculins, proteins involved in cell-cell adhesion in liquid media.