various plant hosts and plant parts it is capable of colonizing. For example, L. enzymogenes strain C3 (erroneously identified as Stenotrophomonas maltophilia) has been reported to control foliar diseases such as leaf spot of tall fescue caused by Bipolaris sorokiniana, bean rust caused by Uromyces appendiculatus and Fusarium head blight of wheat. L. enzymogenes strain C3 also has been reported to suppress soilborne diseases, such as brown patch in turfgrass caused by Rhizoctonia solani, the seedling disease Pythium damping-off of sugarbeet and summer patch disease of Kentucky bluegrass caused by the root-infecting Magnaporthe poae. Lysobacter sp. SB-K88 has been found to suppress damping-off disease in sugar beet and spinach through antibiosis and characteristic root colonization in perpendicular fashion Islam et al. (2005). Disease-suppressive soils Lysobacter species have also been isolated from soils suppressive to Rhizoctonia solani. Clay soils with natural suppressiveness against Rhizoctonia contained higher numbers of antagonistic isolates of L. gummosus, L. antibioticus, and/or L. capsici. Although the mechanism behind this phenomenon is not yet understood, it appeared that growing grass/clover increased the number of these Lysobacter species, as well as the Rhizoctonia suppressiveness. Mechanisms of antagonism Originally characterized as a biological control agent for plant diseases, L. enzymogenes strain C3 is unique in that it expresses a wide range of mechanisms contributing to microbial antagonism and biological control that are not shared by all strains of the species. The strain produces numerous extracellular enzymes that contribute to biocontrol activity, including multiple forms of β-1,3-glucanases and chitinases. The strain also has been demonstrated to induce systemic resistance in certain plants, protecting them from pathogen infection. In addition, recent studies have indicated important roles for secondary metabolites with antibiotic activity and biosurfactant activity in fungal antagonism. Several of these traits are globally controlled by a regulator encoded by the clp gene. Mutations in clp are intriguing for two reasons. First, the mutant phenotype implies that a broad range of genes is involved in secreted antimicrobials associated with the clp regulon, many of which remain unidentified. The second is that mutations in clp result in significant loss of extracellular enzyme activities and antimicrobial activity displayed by L. enzymogenes strain C3. These activities normally are phenotypically overwhelming and often lead to masking of other phenotypes in standard assays, making mutation effects of non-related genes difficult or nearly impossible to evaluate. However, strains harboring clp gene mutations provide a means to separate clp-regulated