Identification of a new element for RNA replication within the internal ribosome entry site of poliovirus RNA.
Several mutants of the Mahoney strain of poliovirus type 1 have been generated by introducing mutations into the stem-loop II (SLII) structure within the internal ribosomal entry site (IRES). Four of these mutants (SLII-1, -4, -5 and -6 mutants) have been characterized previously and are host-range mutants that replicate well in human HeLa cells but not in mouse cells. Two deletion mutants, SLII-2 and SLII-3, were non-viable, even in HeLa cells. It is now reported that SLII-2 was defective in genome RNA synthesis and viral protein synthesis, while SLII-3 was defective only in viral protein synthesis. These results indicate that the SLII region contains a cis-element for RNA replication as well as for IRES-dependent translation and that these two functions lie at the same sites within the SLII region. The host cellular factors that interacted with wild-type SLII and mutant SLII-2 and SLII-3 RNAs were different, suggesting that different host-factor binding regulates expression of mutant phenotypes.
Ishii
T
T
Shiroki
K
K
Iwai
A
A
Nomoto
A
A
D006367:HeLa Cells; D006801:Humans; D008970:Molecular Weight; D009154:Mutation; D017955:Poliovirus / Q000235:genetics*; D012367:RNA, Viral / Q000096:biosynthesis* / Q000737:chemistry; D012270:Ribosomes / Q000821:virology*
D012367:RNA, Viral