January 15-19, 2005
Town & Country Convention Center
San Diego, CA
Wencai Yang1 , Gitta L. Coaker1 , Michael T. Kinter2 , David M. Francis1
Bacterial Canker of tomato is caused by the Gram-positive bacterium Clavibacter michiganensis subsp. michiganensis (Cmm). The disease is potentially devastating due to systemic spread through the xylem. Partial resistance to Cmm in Lycopersicon hirsutum LA407 is controlled by two QTL, Rcm2.0 and Rcm5.1. Previous studies demonstrate that these two loci interact to explain 60-70% of the phenotypic variation for resistance. Patterns of protein and gene expression in leaf tissue suggest that the QTL mediate resistance through distinct pathways. Data from two-dimensional gel electrophoresis and tandem mass spectrometry of proteins isolated from infected stems support our hypothesis that Rcm 2.0 and Rcm 5.1 mediate resistance through separate but complimentary mechanisms. Pathogenesis-related proteins and enzymes capable of generating oxidants are differentially expressed in resistant and susceptible tomato lines in response to Cmm infection. We searched the Clavibacter michiganensis subsp. sepedonicus (CMS) database for potential virulence factors based on analogy to mammalian pathogenisis by Gram-positive pathogens. Database searches and de novo sequencing identified a furA-catalase operon, shared by CMS and Cmm, with similar structure to a Mycobacterium virulence operon. Both the fur regulator and the catalase genes are transcribed in tomato during infection suggesting that catalase production may be used by Cmm to counter host defense.