Open AccessStreptomyces scabies 87-22 Contains a Coronafacic Acid-Like Biosynthetic Cluster That Contributes to Plant–Microbe Interactions
Author(s) -
Dawn R. D. Bignell,
Ryan F. Seipke,
José C. HuguetTapia,
Alan H. Chambers,
Ronald J. Parry,
Rosemary Loria
Publication year - 2010
Publication title -
molecular plant-microbe interactions
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.565
H-Index - 153
eISSN - 1943-7706
pISSN - 0894-0282
DOI - 10.1094/mpmi-23-2-0161
Subject(s) - virulence , phytotoxin , pseudomonas syringae , biology , gene cluster , streptomyces , microbiology and biotechnology , coronatine , common scab , arabidopsis , genetics , pathogen , gene , mutant , bacteria , toxin
Plant-pathogenic Streptomyces spp. cause scab disease on economically important root and tuber crops, the most important of which is potato. Key virulence determinants produced by these species include the cellulose synthesis inhibitor, thaxtomin A, and the secreted Nec1 protein that is required for colonization of the plant host. Recently, the genome sequence of Streptomyces scabies 87-22 was completed, and a biosynthetic cluster was identified that is predicted to synthesize a novel compound similar to coronafacic acid (CFA), a component of the virulence-associated coronatine phytotoxin produced by the plant-pathogenic bacterium Pseudomonas syringae. Southern analysis indicated that the cfa-like cluster in S. scabies 87-22 is likely conserved in other strains of S. scabies but is absent from two other pathogenic streptomycetes, S. turgidiscabies and S. acidiscabies. Transcriptional analyses demonstrated that the cluster is expressed during plant–microbe interactions and that expression requires a transcriptional regulator embedded in the cluster as well as the bldA tRNA. A knockout strain of the biosynthetic cluster displayed a reduced virulence phenotype on tobacco seedlings compared with the wild-type strain. Thus, the cfa-like biosynthetic cluster is a newly discovered locus in S. scabies that contributes to host–pathogen interactions.