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Ribosomal frameshifting may be controlled by mechanisms found in the mRNA sequence (cis-acting). This generally refers to a slippery sequence, an RNA secondary structure, or both. A −1 frameshift signal consists of both elements separated by a spacer region typically 5–9 nucleotides long. [ 2 ]
The HIV-1 ribosomal frameshift signal requires two cis-acting elements: a heptameric "slippery site" and a downstream secondary RNA structure separated by an 8-nucleotide spacer. [3] [4] The "Slippery Site" in HIV-1 is the heptamer 5'-U UUU UUA-3' (gag ORF indicated by the spaces), where frameshifting occurs.
A slippery sequence is a small section of codon nucleotide sequences (usually UUUAAAC) that controls the rate and chance of ribosomal frameshifting. A slippery sequence causes a faster ribosomal transfer which in turn can cause the reading ribosome to "slip."
Translation can also be affected by ribosomal pausing, which can trigger endonucleolytic attack of the tRNA, a process termed mRNA no-go decay. Ribosomal pausing also aids co-translational folding of the nascent polypeptide on the ribosome, and delays protein translation while it is encoding tRNA. This can trigger ribosomal frameshifting. [8]
The DnaX ribosomal frameshifting element is a RNA element found in the mRNA of the dnaX gene in E. coli. The dnaX gene has two encoded products, tau and gamma, which are produced in a 1:1 ratio. The gamma protein is synthesised due to programmed frameshifting and is shorter than tau.
Frameshifting may also occur during prophase translation, producing different proteins from overlapping open reading frames, such as the gag-pol-env retroviral proteins. This is fairly common in viruses and also occurs in bacteria and yeast (Farabaugh, 1996).
In molecular biology, the coronavirus frameshifting stimulation element is a conserved stem-loop of RNA found in coronaviruses that can promote ribosomal frameshifting.Such RNA molecules interact with a downstream region to form a pseudoknot structure; the region varies according to the virus but pseudoknot formation is known to stimulate frameshifting.
The expression of ODC-AZ requires programmed, ribosomal frameshifting which is modulated according to the cellular concentration of polyamines. High levels of polyamines induce a +1 ribosomal frameshift in the translation of mRNA for the antizyme leading to the expression of a full-length protein.