1Plant Pathology Department, Molecular Cellular & Developmental Biology Program, 351 Bessey Hall Iowa State University, Ames, IA 50011, USA.
2School of Public Health, 140 Warren Hall, University of California, Berkeley, CA 94720, USA.
Abstracts of the papers presented at the 16th Annual Convention and International Symposium of Indian Virological Society on “Management of Vector-Borne Viruses” at International Crops Research Institute for the Semi-Arid Tropics (ICRISAT), Patancheru-502324, Hyderabad, India, February 7–10, 2006.
The RNA genomes of many viruses, including the economically important, aphid-transmitted Barley yellow dwarf virus (BYDV, Luteoviridae), lack a 5’ m7GpppN cap, yet they translate efficiently. BYDV relies on a cap-independent translation element (BTE) in its 3’ untranslated region (UTR) to promote translation initiation at the 5’ end. The BTE performs two functions: recruits the translation machinery and communicates with the 5’-end. this is an utterly novel translation initiation mechanism. The communication is facilitated by kissing stem-loop base pairing between the BTE and a stem-loop (D) in the 5’ UTR, located four kilobases upstream. Here we determine the tolerated variations in this base pairing. While some complementary sequences were not tolerated, we were able to separate the long-distance base pairing from the translation machinery recruiting function by placing complementary sequences in the 3’ UTR outside of the BTE. We show that the BTE can use the complementary cyclization sequences located at opposite ends of the 10 kb Dengue virus RNA genome (Flaviviridae), to cause the normally capped Dengue virus-derived mRNA to translate cap-independently. We propose that the long-distance base pairing provides a molecular traffic signal to turn off translation and permit replication of the viral genome. The viral replicase, moving in the 5’ direction while copying the 3’ end of the genomic RNA template, can disrupt translation far upstream to free the genome of ribosomes that would impede the replicase. This provides an elegant mechanism that ensures the balance of translation and replication necessary to maintain a productive infection.
