Fig. 3.

Trans-regulation model of BYDV gene expression. A. Early in infection, when few viral genomes are present, the BTE binds the eIF4G subunit of the key translation initiation factor, eIF4F and delivers it to 5’ end via long-distance base pairing to recruit (or deliver) the 43S ribosomal pre-initiation complex to the 5’ end. The relative excess of eIF4F in the cell facilitates ribosome scanning through the highly structured 5’ UTR. B. Late in infection, the vast excess of sgRNA2 binds much of the eIF4F pool, leaving fewer eIF4F complexes available for translation of gRNA and sgRNA1 (light shaded eIF4E/eIF4G). This allows structure in gRNA 5’ UTR to inhibit ribosome scanning, while 5’ UTR of sgRNA1 has less structure, making it less eIF4F-dependent (Pestova and Kolupaeva, 2002), thus permitting ribosome scanning and translation. Thus sgRNA2 accumulation serves as a switch to inhibit translation of the polymerase from gRNA, and favor translation of structural (CP, CP-RTD) and movement proteins (ORF3a, ORF4) from sgRNA1 (Fig. 1). Details and supporting data are in Shen et al. (Shen et al., 2006).