
Regulators of Viral Frameshifting: More Than RNA Influences Translation Events
Author(s) -
Wesley D. Penn,
Haley R. Harrington,
Jonathan P. Schlebach,
Suchetana Mukhopadhyay
Publication year - 2020
Publication title -
annual review of virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.605
H-Index - 42
eISSN - 2327-0578
pISSN - 2327-056X
DOI - 10.1146/annurev-virology-012120-101548
Subject(s) - translational frameshift , biology , pseudoknot , translation (biology) , rna , messenger rna , protein biosynthesis , translational regulation , genetics , ribosome , translational efficiency , microbiology and biotechnology , gene
Programmed ribosomal frameshifting (PRF) is a conserved translational recoding mechanism found in all branches of life and viruses. In bacteria, archaea, and eukaryotes PRF is used to downregulate protein production by inducing a premature termination of translation, which triggers messenger RNA (mRNA) decay. In viruses, PRF is used to drive the production of a new protein while downregulating the production of another protein, thus maintaining a stoichiometry optimal for productive infection. Traditionally, PRF motifs have been defined by the characteristics of two cis elements: a slippery heptanucleotide sequence followed by an RNA pseudoknot or stem-loop within the mRNA. Recently, additional cis and new trans elements have been identified that regulate PRF in both host and viral translation. These additional factors suggest PRF is an evolutionarily conserved process whose function and regulation we are just beginning to understand.