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Informational suppression as a tool for the investigation of gene structure and function.

Changes in the genetic material that generate nonsense, missense or frameshift mutations may be suppressed by second site lesions in unlinked genes. When partial or total restoration of the wild phenotype is achieved by alteration of the translational apparatus, the process is termed informational suppression. [Phenotypic suppression, on the other hand, refers to suppression by extracellular changes, for example, the presence of streptomycin in the growth medium; reviewed by Gorini (1974).] Informational suppression functions primarily through changes in tRNA species (but see below). Thus, nonsense suppressor tRNAs carry, in general, mutant anticodons capable of base pairing with translation-terminating triplets (sup9 is an exception, see Table 1). They, therefore, prevent premature termination of translation at internal chain-terminating triplets (Fig. 1). In missense suppression, the altered anticodon allows pairing of a tRNA with non-cognate triplets [e.g. tRNA GlT inserts glycine residues at GAG (Glu) codons; reviewed by Hill (1975)1. Of those frameshift suppressor tRNAs sequenced, there is an additional ribonucleotide in the anticodon loop which restores, presumably, the correct reading-frame [reviewed by Roth (1974)]. This ability to perturb the course of gene expression allows both the analysis of the translation decoding mechanism and the creation of protein variants carrying known amino acid substitutions at defined sites. This review is concerned with such applications of nonsense suppression. Suppression has been previously reviewed by Garen (1968), Brammar (1969), Gorini (1970), Hartman & Roth (1973), Smith (1979) and Steege & S611 (1979) (prokaryotes), and by Hawthorne & Leupold (1974), Piper (1980), Olson et al. (1980, Kohli et al. (1980) and Sherman (1982) (eukaryotes).