TY - JOUR

T1 - trans complementation of cap-independent translation directed by poliovirus 5′ noncoding region deletion mutants

T2 - Evidence for RNA-RNA interactions

AU - Stone, David M.

AU - Almond, Jeffrey W.

AU - Brangwyn, Julia K.

AU - Belsham, Graham J.

PY - 1993/10

Y1 - 1993/10

N2 - Poliovirus (PV) RNA is translated by a cap-independent mechanism involving the internal entry of ribosomes onto the 5′ noncoding region (NCR). Using the vaccinia virus-T7 RNA polymerase transient expression system, we showed previously that deletion of certain individual predicted secondary structures within the PV 5′ NCR rendered the element defective in directing internal initiation when assayed alone. However, these defective 5′ NCRs were functional when coexpressed within cells with full-length PV cDNA (N. Percy, G. J. Belsham, J. K. Brangwyn, M. Sullivan, D. M. Stone, and J. W. Almond, J. Virol. 66:1695-1701, 1992). We have extended the study to demonstrate that when these predicted secondary structures are deleted in combination, the enhanced activity in the presence of the full-length PV cDNA is still observed. Indeed, a poliovirus 5′ NCR devoid of all predicted secondary structures is capable of initiating protein synthesis under these conditions. Surprisingly, we also found that this enhancement of activity requires neither any PV protein nor the inhibition of cap-dependent translation. The results indicate that the defective PV 5′ NCR elements can be complemented in trans by functional 5′ NCRs in a highly sequence specific manner.

AB - Poliovirus (PV) RNA is translated by a cap-independent mechanism involving the internal entry of ribosomes onto the 5′ noncoding region (NCR). Using the vaccinia virus-T7 RNA polymerase transient expression system, we showed previously that deletion of certain individual predicted secondary structures within the PV 5′ NCR rendered the element defective in directing internal initiation when assayed alone. However, these defective 5′ NCRs were functional when coexpressed within cells with full-length PV cDNA (N. Percy, G. J. Belsham, J. K. Brangwyn, M. Sullivan, D. M. Stone, and J. W. Almond, J. Virol. 66:1695-1701, 1992). We have extended the study to demonstrate that when these predicted secondary structures are deleted in combination, the enhanced activity in the presence of the full-length PV cDNA is still observed. Indeed, a poliovirus 5′ NCR devoid of all predicted secondary structures is capable of initiating protein synthesis under these conditions. Surprisingly, we also found that this enhancement of activity requires neither any PV protein nor the inhibition of cap-dependent translation. The results indicate that the defective PV 5′ NCR elements can be complemented in trans by functional 5′ NCRs in a highly sequence specific manner.

UR - http://www.scopus.com/inward/record.url?scp=0027323270&partnerID=8YFLogxK

M3 - Journal article

C2 - 8396677

AN - SCOPUS:0027323270

VL - 67

SP - 6215

EP - 6223

JO - Journal of Virology

JF - Journal of Virology

SN - 0022-538X

IS - 10

ER -