Escherichia coli DH5a was used to amplify plasmid DNA. Transformation of E. coli and yeast, and preparation of yeast growth media (YPAD, synthetic drop out medium, and 4.7 MB plates for testing the Killer phenotype) were as reported earlier (18) . Restriction enzymes were obtained from MBI Fermentas (Vilnius, Lithuania). The QuikChange XL II site-directed specific mutagenesis kit was obtained from Stratagene (La Jolla, CA, USA). Macrogen Inc. (Piscataway, NJ, USA) performed DNA sequence analysis. Oligonucleotide primers were purchased from IDT (Coralville, IA, USA). The yeast strains used in this study were all derived from the rpl3-gene disruption (rpl3D) strain JD1090 (MAT ura3-52 lys2-801 trp1 leu2 À his3 RPL3::HIS3 pRPL3-URA3-CEN6 [L-A HN M 1 ]) (19) . Mutants of rpl3 were generated using the wild-type RPL3 gene in pJD225 (19) , synthetic oligonucleotides, and the QuikChange XL II kit. The pYDL dual luciferase reporter series of plasmids for monitoring programmed ribosomal frameshifting (PRF) were used as described earlier (20) . (36) . L3 is indicated in green. The aa-tRNA accommodation corridor is framed by Helix 89, and the complex structure formed by Helices 90-92. Elongation factors bind to the GTPase Associated Center (GAC) and the Sarcin/Ricin Loop (SRL) at the tip of Helix 95. The peptidyltransferase center (PTC) is in the center of the large subunit. (B) The 3D view of isolated L3, heat map colored from the N-terminus (blue) to the C-terminus (red). The N-terminal extension and the basic thumb and tryptophan (W) finger of the central extension are indicated. (C) The 3D view of interactions between amino acid residues of the L3 basic thumb investigated in this study. It is surrounded by a cagelike structure formed by 25S rRNA Helices 61-64, H73 and H90. Amino acids mutated in this study are labeled.