RESUMO
In response to nitrogen limitation, diploid yeast strains of Saccharomyces cerevisiae undergo a dimorphic transition to a filamentous growth form known as pseudohyphal growth. This developmental change can be classified into two distinct growing forms: invasive pseudohyphal growth and superficial pseudohyphal growth. We identified a yeast gene, SFG1, whose overexpression predominantly enhances superficial pseudohyphal growth when starved for nitrogen. Sfg1 has a sequence similarity to members of a family of transcriptional regulators of fungal development. Cells of a homozygous sfg1/sfg1 diploid strain have a serious defect in pseudohyphal growth, indicating that Sfg1 has an essential function for pseudohyphal development. Our analyses show that Sfg1 may act separately from mitogen-activated protein kinase (MAPK) pathway and cAMP-dependent protein kinase A (PKA) pathway.
Assuntos
Genes Fúngicos , Proteínas de Saccharomyces cerevisiae/genética , Saccharomyces cerevisiae/crescimento & desenvolvimento , Sequência de Aminoácidos , Sistema de Sinalização das MAP Quinases , Dados de Sequência Molecular , Saccharomyces cerevisiae/genética , Proteínas de Saccharomyces cerevisiae/química , Homologia de Sequência de Aminoácidos , beta-Galactosidase/genéticaRESUMO
In Saccharomyces cerevisiae, cell type determines two distinct spatial budding patterns. Haploid cells exhibit an axial pattern, whereas diploid cells exhibit a bipolar pattern. Axl1, a member of the insulin-degrading enzyme (IDE) family, is the key morphological determinant for the haploid axial pattern. Here we identified a novel gene, RAX1, specifically required for the bipolar budding pattern. Loss of RAX1 alters the bipolar pattern of axl1 haploids resulting in reversion to the axial pattern, and also alters the bipolar patterns of bud3 and bud4 haploids. However, bud10 rax1 haploids exhibit a random budding pattern, suggesting Bud10 acts as the key proximal landmark in axial budding. Rax1 is required for the localization of Bud8, the distal bipolar budding landmark. Interestingly, Rax1 contains a C-terminal domain possessing some similarity to insulin-related peptides. Our results suggest that Rax1 is necessary for the establishment of the bipolar budding landmark.
