Key result
The co-opted cellular DDX3-like Ded1 DEAD-box helicase suppresses tombusviral RNA recombination in yeast, and its depletion leads to a 5-fold increase in viral recombinant RNA accumulation.
Effect estimate: ~5-fold increase with depletion
The co-opted cellular DEAD-box helicase Ded1 suppresses viral RNA recombination and maintains viral genome integrity during replication.
Cellular helicases may curb viral RNA diversity in models; extends host factor roles in recombination but leaves open mammalian relevance.
The intricate interactions between viruses and hosts include an evolutionary arms race and adaptation that is facilitated by the ability of RNA viruses to evolve rapidly due to high frequency mutations and genetic RNA recombination. In this paper, we show evidence that the co-opted cellular DDX3-like Ded1 DEAD-box helicase suppresses tombusviral RNA recombination in yeast model host, and the orthologous RH20 helicase functions in a similar way in plants. In vitro replication and recombination assays confirm the direct role of the ATPase function of Ded1p in suppression of viral recombination. We also present data supporting a role for Ded1 in facilitating the switch from minus- to plus-strand synthesis. Interestingly, another co-opted cellular helicase, the eIF4AIII-like AtRH2, enhances TBSV recombination in the absence of Ded1/RH20, suggesting that the coordinated actions of these helicases control viral RNA recombination events. Altogether, these helicases are the first co-opted cellular factors in the viral replicase complex that directly affect viral RNA recombination. Ded1 helicase seems to be a key factor maintaining viral genome integrity by promoting the replication of viral RNAs with correct termini, but inhibiting the replication of defective RNAs lacking correct 5' end sequences. Altogether, a co-opted cellular DEAD-box helicase facilitates the maintenance of full-length viral genome and suppresses viral recombination, thus limiting the appearance of defective viral RNAs during replication.
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Chuang et al. (2015) studied Viral RNA recombination (Tomato bushy stunt virus). Ded1p / AtRH20 DEAD-box helicases vs. Depleted or mutant helicase was evaluated on Accumulation of viral recombinant RNAs (recRNAs) (~5-fold increase with depletion). The co-opted cellular DDX3-like Ded1 DEAD-box helicase suppresses tombusviral RNA recombination in yeast, and its depletion leads to a 5-fold increase in viral recombinant RNA accumulation.
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