Reference: Valerius O, et al. (2007) The Saccharomyces homolog of mammalian RACK1, Cpc2/Asc1p, is required for FLO11-dependent adhesive growth and dimorphism. Mol Cell Proteomics 6(11):1968-79

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Abstract


Nutrient starvation results in the interaction of Saccharomyces cerevisiae cells with each other and with surfaces. Adhesive growth requires the expression of the FLO11 gene regulated by the Ras/cAMP/cAMP-dependent protein kinase, the Kss1p/MAPK, and the Gcn4p/general amino acid control pathway, respectively. Proteomics two-dimensional DIGE experiments revealed post-transcriptionally regulated proteins in response to amino acid starvation including the ribosomal protein Cpc2p/Asc1p. This putative translational regulator is highly conserved throughout the eukaryotic kingdom and orthologous to mammalian RACK1. Deletion of CPC2/ASC1 abolished amino acid starvation-induced adhesive growth and impaired basal expression of FLO11 and its activation upon starvation in haploid cells. In addition, the diploid Flo11p-dependent pseudohyphal growth during nitrogen limitation was CPC2/ASC1-dependent. A more detailed analysis revealed that a CPC2/ASC1 deletion caused increased sensitivity to cell wall drugs suggesting that the gene is required for general cell wall integrity. Phosphoproteome and Western hybridization data indicate that Cpc2p/Asc1p affected the phosphorylation of the translational initiation factors eIF2 alpha and eIF4A and the ribosome-associated complex RAC. A crucial role of Cpc2p/Asc1p at the ribosomal interface coordinating signal transduction, translation initiation, and transcription factor formation was corroborated.

Reference Type
Journal Article | Research Support, Non-U.S. Gov't
Authors
Valerius O, Kleinschmidt M, Rachfall N, Schulze F, López Marín S, Hoppert M, Streckfuss-Bömeke K, Fischer C, Braus GH
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