Finally, the ability to direct ribosomes to the +1 reading frame in living cells ( Figure 6 ) suggests a potential therapeutic application for antisense oligonucleotides. Directed frameshifting to the +1 reading frame near a disease causing À1 frameshift mutation would cause some ribosomes to resume decoding in the wild-type ORF, thus restoring partial production of full-length protein from mutant alleles. The importance of the stop codon for efficient frameshifting suggests that the stop codon following the frameshift mutation presents a promising target for antisense induced phenotypic suppression, and that modulation of intracellular polyamine levels, although not essential, may increase the effectiveness of this approach. Further experiments are required to determine the therapeutic potential of this approach in vivo including the generality and efficiency of frameshift induction at non-programmed frameshift sites. The gene of an archaeal α-l-fucosidase is expressed by translational frameshifting The standard rules of genetic translational decoding are altered in specific genes by different events that are globally termed recoding. In Archaea recoding has been unequivocally determined so far only for termination codon readthrough events. We study here the mechanism of expression of a gene encoding for a α-l-fucosidase from the archaeon Sulfolobus solfataricus (fucA1), which is split in two open reading frames separated by a −1 frameshifting. The expression in Escherichia coli of the wild-type split gene led to the production by frameshifting of full-length polypeptides with an efficiency of 5%. Mutations in the regulatory site where the shift takes place demonstrate that the expression in vivo occurs in a programmed way. Further, we identify a full-length product of fucA1 in S.solfataricus extracts, which translate this gene in vitro by following programmed −1 frameshifting. This is the first experimental demonstration that this kind of recoding is present in Archaea. Translation is optimally accurate and the correspondence between the nucleotide and the protein sequences are often considered as an immutable dogma. However, the genetic code is not quite universal: in certain organelles and in a small number of organisms the meaning of different codons has been reassigned and all the mRNAs are decoded accordingly. More surprisingly, the standard rules of genetic decoding are altered in specific genes by different events that are globally termed recoding (1) . In all cases, translational recoding occurs in competition with normal decoding, with a proportion of the ribosomes not obeying to the 'universal' rules. Translational recoding has been identified in both prokaryotes and eukaryotes. It has crucial roles in the regulation of gene expression and includes stop codon readthrough, ribosome hopping and ±1 programmed frameshifting [for reviews see (2) (3) (4) ].