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 to each other and to surfaces. Adhesive growth requires the expression of the FLO11 gene regulated by the Ras/cAMP/PKA, the Kss1p/MAPK, and the Gcn4p/general amino acid control pathway, respectively. Proteomic 2D-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 abolishes amino acid starvation-induced adhesive growth and impairs basal expression of FLO11 and its activation upon starvation in haploid cells. In addition, the diploid Flo11p-dependent pseudohyphal growth during nitrogen limitation is CPC2/ASC1-dependent. A more detailed analysis revealed that a CPC2/ASC1 deletion causes increased sensitivity to cell wall drugs suggesting that the gene is required for general cell wall integrity. Phosphoproteome and Western hybridisation data indicate that Cpc2p/Asc1p affects the phosphorylation of the translational initiation factors eIF2alpha and eIF4A and the ribosomal associated complex RAC. A crucial role of Cpc2p/Asc1p at the ribosomal interface coordinating signal transduction, translation initiation, and transcription factor formation, is corroborated.

Reference Type
Journal Article
Authors
Valerius O, Kleinschmidt M, Rachfall N, Schulze F, Lopez Marin S, Hoppert M, Streckfuss-Bomeke K, Fischer C, Braus GH
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