The activity of Rhizobium japonicum against the soil-borne pathogens Fusarium solani and Macrophomina phaseolina as causative agents of soybean root rot disease in both culture medium and soil was evaluated. Rhizobial culture filtrate caused an inhibition of the fungal radial growth of Fusarium solani and Macrophomina phaseolina on potato dextrose agar medium amended with the filtrate compared with control. The addition of rhizobial culture suspension to the soil contaminated by the two pathogens, Fusarium solani and Macrophomina phaseolina and their interaction, in pots, improved seed germination percentages and reduced the root rot disease index significantly. The sowing of rhizobial coated seeds in soil contaminated by Fusarium solani and Macrophomina phaseolina separately and in combination, in the field, increased seed germination significantly and induced a high reduction in disease severity for the same previous combination under field conditions. These results indicate that rhizobia could be an important element in root rot disease management.

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Arabidopsis thaliana ecotype En-2 is resistant to several strains of Cauliflower mosaic virus (CaMV), including strain W260, but is susceptible to strain NY8153. Resistance in En-2 is conditioned by a single, semi-dominant gene called CAR1. We constructed several recombinant infectious clones between W260 and NY8153 and evaluated their capability to infect En-2. This analysis showed that the capacity of NY8153 to break resistance in En-2 was conditioned by mutations within the CaMV gene 1, a gene that encodes a protein dedicated to cell-to-cell movement (P1), and conversely, that P1 of W260 is responsible for eliciting the plant defense response. A previous study had shown that P6 of W260 was responsible for overcoming resistance in Arabidopsis ecotype Tsu-0 and that P6 of CaMV strain CM1841 was responsible for triggering resistance. The present study now shows that a second gene of CaMV is targeted by Arabidopsis for plant immunity.

In this paper we have characterized the lineage of two traits associated with the coat proteins (CPs) of the tombusvirids: Silencing suppression and HR elicitation in Nicotiana species. We considered that the tombusvirid CPs might collectively be considered an effector, with the CP of each CP-encoding species comprising a structural variant within the family. Thus, a phylogenetic analysis of the CP could provide insight into the evolution of a pathogen effector. The phylogeny of the CP of tombusvirids indicated that CP representatives of the family could be divided into four clades. In two separate clades the CP triggered a hypersensitive response (HR) in Nicotiana species of section Alatae but did not have silencing suppressor activity. In a third clade the CP had a silencing suppressor activity but did not have the capacity to trigger HR in Nicotiana species. In the fourth clade, the CP did not carry either function. Our analysis illustrates how structural changes that likely occurred in the CP effector of progenitors of the current genera led to either silencing suppressor activity, HR elicitation in select Nicotiana species, or neither trait.