作者: Rasmus Torbensen , Henrik Devitt Møller , David Gresham , Sefa Alizadeh , Doreen Ochmann
DOI: 10.1371/JOURNAL.PONE.0041272
关键词:
摘要: Amino acids can induce yeast cell adhesion but how amino are sensed and signal the modulation of FLO genes is not clear. We discovered that budding Saccharomyces cerevisiae CEN.PK evolved invasive growth ability under prolonged nitrogen limitation. Such mutants were used to identify acid transporters as regulators FLO11 growth. One mutant had elevated levels mRNA a Q320STOP mutation in SFL1 gene encodes protein kinase A pathway regulated repressor FLO11. Glutamine-transporter DIP5 GNP1 essential for expression, biofilm formation this mutant. Invasive relied on known Ssy1-Ptr3-Ssy5 complex controls GNP1, suggesting Dip5 Gnp1 operates downstream regulation expression dependent manner. The role appears be conserved S. strain ∑1278b since dip5 gnp1 showed no phenotype. Secondly, transporter GAP1 was found influence through well other genes. Cells carrying dominant loss-of-function PTR3647::CWNKNPLSSIN allele increased transcription FLO1, 5, 9, 10, 11 GAP1. Deletion caused loss However, deletions encoding components mitogen-activated or sufficient abolish growth, involvement alternative pathways. Increased intracellular pools PTR3647::CWNKNPLSSIN-containing opens possibility Gap1 regulates alteration pool sizes.