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1 Department of Cell Biology and Molecular Genetics, University of Maryland, College Park, Maryland 20742, USA
2 Department of Molecular Genetics and Microbiology, and The Graduate Programs in and Molecular Bioscience Rutgers/University of Medicine and Dentistry of New Jersey, Robert Wood Johnson Medical School, Piscataway, New Jersey 08854, USA
Reprint requests to: Jonathan D. Dinman, Department of Cell Biology and Molecular Genetics, Microbiology Bldg. Rm. 2135, University of Maryland, College Park, MD 20742, USA; e-mail: jd280{at}umail.umd.edu..
There is something special about mRNA pseudoknots that allows them to elicit efficient levels of programmed –1 ribosomal frameshifting. Here, we present a synthesis of recent crystallographic, molecular, biochemical, and genetic studies to explain this property. Movement of 9 Å by the anticodon loop of the aminoacyl-tRNA at the accommodation step normally pulls the downstream mRNA a similar distance along with it. We suggest that the downstream mRNA pseudoknot provides resistance to this movement by becoming wedged into the entrance of the ribosomal mRNA tunnel. These two opposing forces result in the creation of a local region of tension in the mRNA between the A-site codon and the mRNA pseudoknot. This can be relieved by one of two mechanisms; unwinding the pseudoknot, allowing the downstream region to move forward, or by slippage of the proximal region of the mRNA backwards by one base. The observed result of the latter mechanism is a net shift of reading frame by one base in the 5' direction, that is, a –1 ribosomal frameshift.
Keywords: Virus; ribosome; translation; genetic code; recoding; structure/function
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