Chemical compounds from Dictyostelium discoideum repel a plant-parasitic nematode and can protect roots.

Slime mold species in the genus Dictyostelium are considered to have a close relationship with non-parasitic nematodes; they are sympatric in soils and can exhibit interspecific competition for food. We investigated whether this relationship extends to a plant-parasitic nematode that is active in the rhizosphere and has broad host specificity, damaging crops worldwide. Using a novel assay to examine the interaction between the cellular slime mold, Dictyostelium discoideum, and the plant-parasitic nematodes, Meloidogyne spp., we found that cellular slime molds can repel plant parasitic nematodes. Specifically, the repulsion activity was in response to chemical compounds released by cellular slime mold fruiting bodies. Under laboratory conditions, these soluble chemical extracts from fruiting bodies of D. discoideum showed repulsion activity strong enough to protect plant roots. The fruiting body cell extracts repelled but were not toxic to the plant-parasitic nematodes

Mutation in the Threonine Synthase Gene Results in an Over-Accumulation of Soluble Methionine in Arabidopsis

In higher plants, O-phosphohomoserine (OPH) represents a branch point between the methionine (Met) and threonine (Thr) biosynthetic pathways. It is believed that the enzymes Thr synthase (TS) and cystathionine γ-synthase (CGS) actively compete for the OPH substrate for Thr and Met biosynthesis, respectively. We have isolated a mutant of Arabidopsis, designated mto2-1, that over-accumulates soluble Met 22-fold and contains markedly reduced levels of soluble Thr in young rosettes. The mto2-1 mutant carries a single base pair mutation within the gene encoding TS, resulting in a leucine-204 to arginine change. Accumulation of TS mRNA and protein was normal in young rosettes of mto2-1, whereas functional complementation analysis of an Escherichia coli thrC mutation suggested that the ability of mto2-1 TS to synthesize Thr is impaired. We concluded that the mutation within the TS gene is responsible for the mto2-1 phenotype, resulting in decreased Thr biosynthesis and a channeling of OPH to Met biosynthesis in young rosettes. Analysis of the mto2-1 mutant suggested that, in vivo, the feedback regulation of CGS is not sufficient alone for the control of Met biosynthesis in young rosettes and is dependent on TS activity. In addition, developmental analysis of soluble Met and Thr concentrations indicated that the accumulation of these amino acids is regulated in a temporal and spatial manner