Clavibacter michiganensis subsp. nebraskensis causes Goss’s bacterial wilt and blight on maize and is managed primarily with C. michiganensis subsp. nebraskensis-resistant hybrids. To understand the mechanisms of resistance to infection by C. michiganensissubsp. nebraskensis, leaves of a susceptible and a resistant maize hybrid at the V4 to V5 developmental stage were wound inoculated with the pathogen. Blight lesion length was monitored, C. michiganensis subsp. nebraskensis colonizing ability was determined, and structural changes were observed using microscopy. Bacterial colonization preceded lesion development that occurred 4 to 5 days postinoculation in both hybrids. Lesion expansion in the susceptible hybrid was associated with a faster rate of C. michiganensis subsp. nebraskensis spread and multiplication in the tissues. In the resistant hybrid, spread and multiplication was reduced (P < 0.0001) and, at 16 days postinoculation, became imperceptible. Initially, C. michiganensis subsp. nebraskensis showed a preference for colonization of the metaxylem vessels in both hybrids. Spread from cell to cell was accomplished through disruption of cell walls, presumably from abundance of bacterial cells or enzymatic activity. Morphological responses of the resistant maize hybrid to infection by C. michiganensis subsp. nebraskensis were similar to those reported in maize inbred lines that were resistant to Stewart’s wilt caused by Pantoea stewartii. Resistance to C. michiganensis subsp. nebraskensis was associated with production of a dense matrix in the xylem that deformed and restricted movement of the bacterial cells.
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