Genomic expression patterns in cell separation mutants of Schizosaccharomyces pombe defective in the genes sep10 ( + ) and sep15 ( + ) coding for the Mediator subunits Med31 and Med8.

Cell division is controlled by a complex network involving regulated transcription of genes and postranslational modification of proteins. The aim of this study is to demonstrate that the Mediator complex, a general regulator of transcription, is involved in the regulation of the second phase (cell separation) of cell division of the fission yeast Schizosaccharomyces pombe. In previous studies we have found that the fission yeast cell separation genes sep10 ( + ) and sep15 ( + ) code for proteins (Med31 and Med8) associated with the Mediator complex. Here, we show by genome-wide gene expression profiling of mutants defective in these genes that both Med8 and Med31 control large, partially overlapping sets of genes scattered over the entire genome and involved in diverse biological functions. Six cell separation genes controlled by the transcription factors Sep1 and Ace2 are among the target genes. Since neither sep1 ( + ) nor ace2 ( + ) is affected in the mutant cells, we propose that the Med8 and Med31 proteins act as coactivators of the Sep1-Ace2-dependent cell separation genes. The results also indicate that the subunits of Mediator may contribute to the coordination of cellular processes by fine-tuning of the expression of larger sets of genes.

Morphology transition genes in the dimorphic fission yeast Schizosaccharomyces japonicus.

The ability of the saprophytic fungus Schizosaccharomyces japonicus to alternate between unicellular yeast form and multicellular true mycelium makes this organism an attractive non-pathogenic model for the investigation of di- and polymorphism critical for pathogenicity in many pathogenic fungi. In a previous work we described three mutations that made the cells unable to form hyphae. Here we report on the isolation of additional mycelium-minus mutants and show that the mutations represent seven genes. Apart from the inhibition of the yeast-to-mycelium transition, the mutations also cause drastic changes in the yeast phase. Cells of myc3-34 and myc4-35 grow isotropically with apolar distribution of actin and randomised localisation of division planes. The mutants myc1-4, myc1-10, myc1-36, myc5-39 and myc6-43 form sep-like, branching microhyphae containing bipolarly growing cells. All mutants are defective in the polarisation of vacuole distribution, and myc3-34, myc4-35 and myc7-56 are also defective in vacuole fusion. The diversity of the mutant phenotypes indicates that several cellular processes must take place simultaneously for the transition from the yeast phase into the mycelial phase.