Interaction of VSV leader RNA and nucleocapsid protein may control VSV genome replication.
The discovery of plus- and minus-strand leader RNAs (short RNAs that are the complement of the exact 3' ends of the viral minus-strand genome and plus-strand antigenome) in VSV-infected cells has led to a model of genome replication in which the viral nucleocapsid protein acts as a modulator of genome transcription and replication. In this model, the VSV leader RNAs are the result of chain termination at an attenuation signal located approximately 50 nucleotides in from the 3' ends of the genome templates. The viral N protein is thought to modulate transcription and replication by its ability to bind to the nascent leader RNA and simultaneously promote read-through of the termination signal and initiate nucleocapsid assembly on the nascent RNA chain. Two predictions of this model, namely, that the requirement of continuous protein synthesis for genome replication is not at the level of the initiation of the genome chains but at the level of the suppression of the leader RNA termination signal, and that the site for the initiation of nucleocapsid assembly is located within the leader RNA sequence, have been tested experimentally and the results found to be consistent with the above model.
D002213:Capsid / Q000235:genetics* / Q000378:metabolism; D008970:Molecular Weight; D011485:Protein Binding; D012367:RNA, Viral / Q000235:genetics* / Q000378:metabolism; D012261:Ribonucleoproteins / Q000235:genetics; D014721:Vesicular stomatitis Indiana virus / Q000235:genetics* / Q000648:ultrastructure; D014764:Viral Proteins / Q000235:genetics*; D014779:Virus Replication
D012367:RNA, Viral; D012261:Ribonucleoproteins; D014764:Viral Proteins