
Posttranscriptional regulation of FLO11 upon amino acid starvation in Saccharomyces cerevisiae
Author(s) -
Fischer Claudia,
Valerius Oliver,
Rupprecht Heike,
Dumkow Marc,
Krappmann Sven,
Braus Gerhard H.
Publication year - 2008
Publication title -
fems yeast research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.991
H-Index - 92
eISSN - 1567-1364
pISSN - 1567-1356
DOI - 10.1111/j.1567-1364.2007.00331.x
Subject(s) - biology , saccharomyces cerevisiae , derepression , biochemistry , psychological repression , amino acid , mutant , transcription (linguistics) , gene , gene expression , microbiology and biotechnology , linguistics , philosophy
Various starvation conditions cause adhesive growth of haploid cells or pseudohyphae formation of diploid cells of Saccharomyces cerevisiae . For the genetic Σ1278b background, these morphological changes depend on the expression of the gene encoding the cell wall glycoprotein Flo11p, which is increased during nutritional limitations. Deletion of the genes encoding the transcriptional coactivators Rsc1p or Gcn5p impairs FLO11 transcription, which consequently leads to a loss of both haploid invasive growth and diploid pseudohyphae development upon glucose and nitrogen limitation, respectively. In contrast, amino acid starvation induces FLO11 ‐dependent adhesive growth of the rsc1 Δ and gcn5 Δ strains although FLO11 transcription remains very low. The double deletion strain rsc1 Δ flo11 Δ, however, does not grow adhesively, suggesting that the adhesion of the rsc1 Δ strain at amino acid starvation is still FLO11 ‐dependent. The FLO11 prom ‐lacZ ‐encoded β‐galactosidase activities of the rsc1 Δ and gcn5 Δ mutant strains increase manifold upon amino acid starvation. It is therefore concluded that low levels of FLO11 transcripts are essential and sufficient for derepression of FLO11 expression and adhesive growth during amino acid starvation. A posttranscriptional control is assumed to be behind this phenomenon that permits the increased FLO11 expression from low FLO11 transcript abundances.