Identification of a complex genetic network underlying Saccharomyces cerevisiae colony morphology.

When grown on solid substrates, different microorganisms often form colonies with very specific morphologies. Whereas the pioneers of microbiology often used colony morphology to discriminate between species and strains, the phenomenon has not received much attention recently. In this study, we use a genome-wide assay in the model yeast Saccharomyces cerevisiae to identify all genes that affect colony morphology.

Variable tandem repeats accelerate evolution of coding and regulatory sequences.

Genotype-to-phenotype mapping commonly focuses on two major classes of mutations: single nucleotide polymorphisms (SNPs) and copy number variation (CNV). Here, we discuss an underestimated third class of genotypic variation: changes in microsatellite and minisatellite repeats. Such tandem repeats (TRs) are ubiquitous, unstable genomic elements that have historically been designated as nonfunctional "junk DNA" and are therefore mostly ignored in comparative genomics.

Unstable tandem repeats in promoters confer transcriptional evolvability.

Relative to most regions of the genome, tandemly repeated DNA sequences display a greater propensity to mutate. A search for tandem repeats in the Saccharomyces cerevisiae genome revealed that the nucleosome-free region directly upstream of genes (the promoter region) is enriched in repeats. As many as 25% of all gene promoters contain tandem repeat sequences.

FLO1 is a variable green beard gene that drives biofilm-like cooperation in budding yeast.

The budding yeast, Saccharomyces cerevisiae, has emerged as an archetype of eukaryotic cell biology. Here we show that S. cerevisiae is also a model for the evolution of cooperative behavior by revisiting flocculation, a self-adherence phenotype lacking in most laboratory strains.

The morphogenetic regulator Czf1p is a DNA-binding protein that regulates white opaque switching in Candida albicans.

Czf1p has been demonstrated to regulate the switch between the yeast-cell morphology and filamentous morphologies of the human fungal pathogen Candida albicans. The predicted amino acid sequence of Czf1p contains a zinc-cluster motif similar to the DNA-binding domains of proteins such as Saccharomyces cerevisiae Gal4p, suggesting that Czf1p is a DNA-binding protein. Czf1p also demonstrates genetic interaction and a two-hybrid interaction with a second regulator of C.

Expression of the Candida albicans morphogenesis regulator gene CZF1 and its regulation by Efg1p and Czf1p.

The ability of Candida albicans to transit between different cellular morphologies is believed to be important for virulence. Morphological transitions occur in response to a variety of environmental signals. One such signal is encountered when cells are grown in a semisolid matrix.

Contributions of hyphae and hypha-co-regulated genes to Candida albicans virulence.

The fascinating ability of Candida albicans to undergo dramatic changes in cellular morphology has invited speculation that this plasticity in form contributes to the virulence of the organism. Molecular genetic analyses have confirmed this hypothesis and further demonstrated that genes that govern cellular morphology are co-regulated with genes encoding conventional virulence factors such as proteases and adhesins. The transcriptional regulatory networks of C.

Alternative Candida albicans lifestyles: growth on surfaces.

Candida albicans, an opportunistic fungal pathogen, causes a wide variety of human diseases such as oral thrush and disseminated candidiasis. Many aspects of C. albicans physiology have been studied during liquid growth, but in its natural environment, the gastrointestinal tract of a mammalian host, the organism associates with surfaces.