Posttranscriptional regulation of FLO11 upon amino acid starvation in Saccharomyces cerevisiae


  • Present address: Claudia Fischer, DSMZ-German Collection of Microorganisms and Cell Cultures, Department of Human and Animal Cell Cultures, Braunschweig, Germany.

  • Editor: Isak Pretorius

Correspondence: Gerhard H. Braus, Institute for Microbiology and Genetics, Georg-August-Universität, Grisebachstr. 8, D-37077 Göttingen, Germany. Tel.: +49 551 393 771; fax: +49 551 393 820; e-mail:


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 rsc1Δ and gcn5Δ strains although FLO11 transcription remains very low. The double deletion strain rsc1Δflo11Δ, however, does not grow adhesively, suggesting that the adhesion of the rsc1Δ strain at amino acid starvation is still FLO11-dependent. The FLO11prom-lacZ-encoded β-galactosidase activities of the rsc1Δ and gcn5Δ 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.