Abstract
Pseudomonas cichorii causes necrotic lesions in eggplant and rot in lettuce. Through transposon insertion into P. cichorii strain SPC9018 we produced two mutants, 4-57 and 2-99, that lost virulence on eggplant but not lettuce. Analyses showed that a transposon was inserted into the hrpG gene in 4-57 and the hrcT gene in 2-99. Nucleotide sequences of the hrp genes of SPC9018 are homologous to those of Pseudomonas viridiflava BS group strains. The pathogenicity of 4-57 on eggplant was restored by transformation with an hrpF operon, originating from either SPC9018 or the BS group member P. viridiflava strain 9504 (Pv9504). These data suggested the involvement of hrp genes in the pathogenicity of SPC9018 on eggplant, and functional conservation of hrpF operons between SPC9018 and Pv9504. Both the hrpS mutant and the hrpL mutant were unable to cause necrotic lesions on eggplant leaves but retained their pathogenicity against lettuce. These results suggest that the pathogenicity of P. cichorii is hrp-dependent in eggplant, but not in lettuce.
Highlights
Pseudomonas cichorii causes necrotic leaf spot on eggplants and rot on lettuce
2-99 and 4-57, that were unable to cause necrotic lesions hrp genes and pathogenicity of P. cichorii on eggplant within 7 days of inoculation (Fig. 1a). The mutants retained their ability to cause rot on lettuce leaves, rot symptoms caused by the mutants were delayed compared to those caused by SPC9018 (Fig. 2)
To analyse the involvement of hrpS and hrpL in the pathogenicity of SPC9018, hrpS- and hrpL-deficient mutants were created. Both the hrpS- and the hrpLdeficient mutants lost their virulence on eggplant, in a manner similar to 2-99 and 4-57 (Fig. 1a). Both the hrpS mutant and the hrpL mutant retained their virulence on lettuce leaves, rot symptoms caused by the mutants were delayed compared to those caused by SPC9018 (Figs 1b and2)
Summary
Pseudomonas cichorii causes necrotic leaf spot on eggplants and rot on lettuce. Microscopic observations using lux-marked P. cichorii and an immunofluorescent antibody against the bacteria have shown that the bacteria first invade lettuce head leaves through stomata and colonize intercellular spaces (Hikichi et al, 1996a, 1998). After proliferation in intercellular spaces of the mesophyll, the bacteria spread throughout the whole leaf via the vascular bundle (Hikichi et al, 1996b). The symptoms appear and develop as the bacteria multiply and spread. Our previous studies have shown that de novo protein synthesis in lettuce leaves is required for the development of disease symptoms (Hikichi et al, 1998; Kiba et al, 2006a). The development of disease symptoms is closely associated with programmed cell death (PCD), following heterochromatin aggregation and laddering of genome DNA in the P. cichorii-infected lettuce
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