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 eIF2Ø 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.