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 Previous Article

Microbiology and Molecular Biology Reviews, March 2009, p. 178-210, Vol. 73, No. 1
1092-2172/09/$08.00+0     doi:10.1128/MMBR.00010-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

A Gripping Tale of Ribosomal Frameshifting: Extragenic Suppressors of Frameshift Mutations Spotlight P-Site Realignment

John F. Atkins1* and Glenn R. Björk2*

BioSciences Institute, University College, Cork, Ireland, and Department of Human Genetics, University of Utah, Salt Lake City, Utah,1 Department of Molecular Biology, Umeå University, SE-90187 Umeå, Sweden2

Summary: Mutants of translation components which compensate for both –1 and +1 frameshift mutations showed the first evidence for framing malleability. Those compensatory mutants isolated in bacteria and yeast with altered tRNA or protein factors are reviewed here and are considered to primarily cause altered P-site realignment and not altered translocation. Though the first sequenced tRNA mutant which suppressed a +1 frameshift mutation had an extra base in its anticodon loop and led to a textbook "yardstick" model in which the number of anticodon bases determines codon size, this model has long been discounted, although not by all. Accordingly, the reviewed data suggest that reading frame maintenance and translocation are two distinct features of the ribosome. None of the –1 tRNA suppressors have anticodon loops with fewer than the standard seven nucleotides. Many of the tRNA mutants potentially affect tRNA bending and/or stability and can be used for functional assays, and one has the conserved C74 of the 3' CCA substituted. The effect of tRNA modification deficiencies on framing has been particularly informative. The properties of some mutants suggest the use of alternative tRNA anticodon loop stack conformations by individual tRNAs in one translation cycle. The mutant proteins range from defective release factors with delayed decoding of A-site stop codons facilitating P-site frameshifting to altered EF-Tu/EF1{alpha} to mutant ribosomal large- and small-subunit proteins L9 and S9. Their study is revealing how mRNA slippage is restrained except where it is programmed to occur and be utilized.

* Corresponding author. Mailing address for John F. Atkins: Department of Human Genetics, University of Utah, Salt Lake City, UT 84112. E-mail: atkins{at}genetics.utah.edu. Mailing address for Glenn R. Björk: Department of Molecular Biology, Umeå University, SE-90187 Umeå, Sweden. Phone: 46-90-7856756. Fax: 46-90-772630. E-mail: glenn.bjork{at}molbiol.umu.se

Microbiology and Molecular Biology Reviews, March 2009, p. 178-210, Vol. 73, No. 1
1092-2172/09/$08.00+0     doi:10.1128/MMBR.00010-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.





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