Plant infection by two different viruses induce contrasting changes of vectors fitness and behavior

Abstract Insect-vectored plant viruses can induce changes in plant phenotypes, thus influencing plant?vector interactions in a way that may promote their dispersal according to their mode of transmission (i.e., circulative vs. noncirculative). This indirect vector manipulation requires host?virus?vector coevolution and would thus be effective solely in very specific plant?virus?vector species associations. Some studies suggest this manipulation may depend on multiple factors relative to various intrinsic characteristics of vectors such as transmission efficiency. In anintegrative study, we tested the effects of infection of the Brassicaceae Camelina sativa with the noncirculative Cauliflower mosaic virus (CaMV) or the circulative Turnip yellows virus (TuYV) on the host-plant colonization of two aphid species differing in their virus transmission efficiency: the polyphagous Myzus persicae, efficient vector of both viruses, and the Brassicaceae specialist Brevicoryne brassicae, poor vector of TuYV and efficient vector of CaMV. Results confirmed the important role of virus mode of transmission as plant-mediated effects of CaMV on the two aphid species induced negative alterations of feeding behavior (i.e., decreased phloem sap ingestion) and performance that were both conducive for virus fitness by promoting dispersion after a rapid acquisition. In addition, virus transmission efficiency may also play a role in vector manipulation by viruses as only the responses of the efficient vector to plant-mediated effects of TuYV, that is, enhanced feeding behavior and performances, were favorable to their acquisition and further dispersal. Altogether, this work demonstrated that vector transmission efficiency also has to be considered when studying the mechanisms underlying vector manipulation by viruses. Our results also reinforce the idea that vector manipulation requires coevolution between plant, virus and vector

Structural Insights into Viral Determinants of Nematode Mediated Grapevine fanleaf virus Transmission

Many animal and plant viruses rely on vectors for their transmission from host to host. Grapevine fanleaf virus (GFLV), a picorna-like virus from plants, is transmitted specifically by the ectoparasitic nematode Xiphinema index. The icosahedral capsid of GFLV, which consists of 60 identical coat protein subunits (CP), carries the determinants of this specificity. Here, we provide novel insight into GFLV transmission by nematodes through a comparative structural and functional analysis of two GFLV variants. We isolated a mutant GFLV strain (GFLV-TD) poorly transmissible by nematodes, and showed that the transmission defect is due to a glycine to aspartate mutation at position 297 (Gly297Asp) in the CP. We next determined the crystal structures of the wild-type GFLV strain F13 at 3.0 Å and of GFLV-TD at 2.7 Å resolution. The Gly297Asp mutation mapped to an exposed loop at the outer surface of the capsid and did not affect the conformation of the assembled capsid, nor of individual CP molecules. The loop is part of a positively charged pocket that includes a previously identified determinant of transmission. We propose that this pocket is a ligand-binding site with essential function in GFLV transmission by X. index. Our data suggest that perturbation of the electrostatic landscape of this pocket affects the interaction of the virion with specific receptors of the nematode's feeding apparatus, and thereby severely diminishes its transmission efficiency. These data provide a first structural insight into the interactions between a plant virus and a nematode vector

Differential Requirements of Two recA Mutants for Constitutive SOS Expression in Escherichia coli K-12

Background Repairing DNA damage begins with its detection and is often followed by elicitation of a cellular response. In E. coli, RecA polymerizes on ssDNA produced after DNA damage and induces the SOS Response. The RecA-DNA filament is an allosteric effector of LexA auto-proteolysis. LexA is the repressor of the SOS Response. Not all RecA-DNA filaments, however, lead to an SOS Response. Certain recA mutants express the SOS Response (recAC) in the absence of external DNA damage in log phase cells. Methodology/Principal Findings Genetic analysis of two recAC mutants was used to determine the mechanism of constitutive SOS (SOSC) expression in a population of log phase cells using fluorescence of single cells carrying an SOS reporter system (sulAp-gfp). SOSC expression in recA4142 mutants was dependent on its initial level of transcription, recBCD, recFOR, recX, dinI, xthA and the type of medium in which the cells were grown. SOSC expression in recA730 mutants was affected by none of the mutations or conditions tested above. Conclusions/Significance It is concluded that not all recAC alleles cause SOSC expression by the same mechanism. It is hypothesized that RecA4142 is loaded on to a double-strand end of DNA and that the RecA filament is stabilized by the presence of DinI and destabilized by RecX. RecFOR regulate the activity of RecX to destabilize the RecA filament. RecA730 causes SOSC expression by binding to ssDNA in a mechanism yet to be determined

The Escherichia coli terB sequence affects maintenance of a plasmid with the M13 phage replication origin.

Replication initiated at the bacteriophage M13 origin can be affected by interaction of a properly oriented termination signal terB and the Tus protein. The effect can be alleviated by overproduction of the M13 replication gene protein II

Une protéine clé pour la transmission d'un virus de plante à la pointe des stylets de l'insecte vecteur

Du fait de l'immobilité de leurs hôtes, l'immense majorité des virus de plante utilisent des vecteurs spécifiques pour passer d'un hôte à un autre. Ces "véhicules de transport" sont principalement des arthropodes et en grande majorité des pucerons, qui sont des insectes de type piqueur-suceur. Pour les interactions virus-vecteur, la stratégie la plus communément utilisée par les virus de plante est la transmission dite non circulante, où les particules virales prélevées lors d'un repas dans les cellules infectées seront retenues au niveau de sites d'attachement dans les pièces buccales antérieures de l'insecte sans effectuer de passage à l'intérieur de son organisme. Ces particules virales seront ensuite relarguées de ces sites d'attachement lors de piqûres sur de nouvelles cellules hôtes et induiront ainsi l'infection dans de nouvelles plantes. Si les mécanismes moléculaires de la transmission non circulante sont bien documentés en ce qui concerne le partenaire viral, les sites d'attachement correspondants dans les stylets du vecteur demeurent la principale "boîte noire" pour laquelle aucune donnée n'est disponible. Malgré l'importance de ce mode de transmission, l'existence même d'un récepteur spécifique n'a jamais été prouvée pour aucun virus. Dans une étude très récemment publiée, nous avons localisé précisément le récepteur du Caulifower mosaic virus (CaMV) et déterminé sa nature chimique

A protein key to plant virus transmission at the tip of the insect vector stylet

Hundreds of species of plant viruses, many of them economically important, are transmitted by noncirculative vector transmission (acquisition by attachment of virions to vector mouthparts and inoculation by subsequent release), but virus receptors within the vector remain elusive. Here we report evidence for the existence, precise location, and chemical nature of the first receptor for a noncirculative virus, cauliflower mosaic virus, in its insect vector. Electron microscopy revealed virus-like particles in a previously undescribed anatomical zone at the extreme tip of the aphid maxillary stylets. A novel in vitro interaction assay characterized binding of cauliflower mosaic virus protein P2 (which mediates virus–vector interaction) to dissected aphid stylets. A P2-GFP fusion exclusively labeled a tiny cuticular domain located in the bottom-bed of the common food/salivary duct. No binding to stylets of a non-vector species was observed, and a point mutation abolishing P2 transmission activity correlated with impaired stylet binding. The novel receptor appears to be a nonglycosylated protein deeply embedded in the chitin matrix. Insight into such insect receptor molecules will begin to open the major black box of this scientific field and might lead to new strategies to combat viral spread.This work was funded by a CT1 grant from the Institut National de la Recherche Agronomique Département Santé des Plantes et Environnement (France), a JE77 grant from the Institut National de la Recherche Agronomique Scientific Direction Plantes et Produits du Végétal (France), and Grant AGL2003-07532-C03-01 from the Ministerio de Educación y Ciencia of Spain.Peer reviewe