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 Ded1 p in suppression of viral recombination.

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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 eIF4AI Ii-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. RNA viruses replicate inside cells and they require many cellular factors to complete their infection cycle.

The intricate interactions between viruses and hosts include 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 as well as reassortment of genomic components [1-3]. Interestingly, cellular and environmental factors affect viral RNA recombination, which is a process that joins two or more noncontiguous segments of the same RNA or two separate RNAs together [4,5]. Recombination could alter viral genomes by introducing insertions or duplications, combining new sequences, or leading to deletions or rearrangements. RNA recombination also functions to repair truncated or damaged viral RNA molecules [2,5-7].

Viral RNA recombination can affect virus population dynamics, contribute to virus variability, as well as function in genome repair that maintains the infectivity of RNA viruses [3,4]. Viral RNA recombination is intensively studied with Tomato bushy stunt virus (TBSV), a tombusvirus infecting plants, using yeast (Saccharomyces cerevisiae) model host. TBSV is an outstanding model for both replication and recombination studies [8-12]. Systematic genome-wide screens with TBSV have led to the identification of more than 30 host genes affecting viral RNA recombination in yeast [8,9,13-15]. Among the host factors identified is the cytosolic Xrn1p 5'-to-3' exoribonuclease (Xrn4 in plants) that suppresses TBSV recombination [16-18]. Xrn1p was shown to rapidly degrade cellular endoribonuclease-cleaved TBSV RNAs, termed degRNAs (Fig. The combined effects of cellular exo- and endoribonucleases determine the accumulation of degRNAs, which are especially active in RNA recombination, and thus, these cellular factors affect the frequency of viral RNA recombination events [9,18].

An additional key cellular factor involved in TBSV recombination is Pmr1 [Ca. Shiraz Signature Keygen. sup.++]/[Mn.sup.++] pump that controls [Mn.sup.++] level in the cytosol [15]. Studies revealed that the cytosolic [Mn.sup.++] level could greatly affect the properties/activities of the viral replicase, including its ability to synthesize RNA and switch templates. For example, high [Mn.sup.++] level (in the absence of Pmr1) leads to high frequency RNA recombination in yeast or plant cells as well as in a cell-free TBSV replication assay [15]. A recent systematic screen with TBSV based on a temperature-sensitive (ts) library of yeast mutants (Prasanth and Nagy, unpublished), identified the yeast Ded1p ATP-dependent DEAD-box RNA helicase as a cellular factor affecting TBSV RNA recombination. Ded1p and ten other yeast DEAD-box proteins, which are the largest family of RNA helicases, were also identified as pro-viral factors in TBSV replication in yeast [13,30-35].