Switch from Cap- to Factorless IRES-Dependent 0 and +1 Frame Translation during Cellular Stress and Dicistrovirus Infection

Wang, Qing S.; Jan, Eric

Infection by dicistroviruses leads to a rapid inhibition of host translation concomitant and a switch to viral translation [27, 28] . To mimic these conditions, we treated cells with DTT, PatA, and 4E1RCat, each targeting specific initiation factors. In all cases, IRES dependent translation is stimulated under these conditions in Drosophila cells ( Figure 5 ). Although we cannot completely rule out that stimulation of IRES-mediated translation is due induction of apoptosis at later time points of drug treatment, it is notable that these results are similar to that observed in mammalian and yeast cells yeast cells [17, [38] [39] [40] [41] 43, 46] and are consistent with the property that the IGR IRES does not require factors for ribosome assembly. Using our transfection protocol of reporter bicistronic RNAs, we also find that both CrPV and IAPV IGR IRESs are stimulated during CrPV infection (Figure 6-7) . These results argue that the stimulation of IGR IRES-mediated translation during infection is not due to the replication of viral RNAs simply outcompeting host mRNAs for ribosomes. To our knowledge, this is the first report addressing IGR IRES translation in dicistrovirusinfected cells.