|Hirano, Susan - UNIVERSITY OF WISCONSIN|
|Ostertag, Eric - UNIVERSITY OF WISCONSIN|
|Savage, Stephanie - UNIVERSITY OF WISCONSIN|
|Baker, L - UNIVERSITY OF WISCONSIN|
Submitted to: Applied and Environmental Microbiology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: August 25, 1997
Publication Date: N/A
Interpretive Summary: By studying genes in pathogens that are required for causation of diseases in plants we hope to improve scientific understanding of what is required to cause disease, and hence how such diseases might be controlled. The bacterium Pseudomonas syringae pv. syringae must have a functional lemA gene to cause brown spot lesions on bean. A mutant of this bacterium that lacks a functional lemA gene does not cause brown spot disease of bean, but grows as well as the pathogenic strain from which it was derived on bean leaves in the laboratory. In the field, however, numbers of the mutant declined relative to those of the pathogen, indicating that the mutant was less fit than its parent on leaves.When the mutant was placed on the same plant as the pathogenic strain from which it had been derived, growth and survival of the pathogenic parent were markedly decreased. Thus, inactivation of the lemA gene produced a mutant that neither produced as many pathogenic progeny on leaves nor allowed the pathogen to produce as many progeny when present on the same leaves. Because the amount of disease is related to the numbers of pathogens present on leaves, this may have long term implications for mitigation of the hazard of brown spot disease.
Technical Abstract: In P. syringae pv. syringae, lemA is required for brown spot lesion formation on snap bean and for production of syringomycin and extracellular proteases (15, 33). The lemA mutant NPS3136 (lemA1::Tn5) is indistinguishable from its pathogenic parent B728a in its ability to grow when infiltrated into bean leaves in laboratory assays(33). .We compared population sizes of NPS3136 and B728aN (a Nalr clone of wild type B728a) in two field experiments to determine the effect of inactivation of lemA on fitness of P. syringae pv. syringae. In one experiment, the bacterial strains were spray-inoculated onto the foliage of 25 day-old bean plants. In the other, seeds were inoculated at the time of planting. In both experiments, the strains were applied alone and co- inoculated in a 1:1 ratio. NPS3136 and B728aN achieved similar high population sizes on germinating seeds. However, in association with leaves, population sizes of NPS3136 were diminished relative to B728aN in both experiments. Thus, lemA contributed significantly to fitness of P. syringae pv. syringae in association with bean leaves, but not on germinating seeds under field conditions. When NPS3136 was co- inoculated with B728aN, the mutant behaved as it did when applied alone. However, populations of B728aN in the co-inoculation treatment were much lower than when inoculated alone. Inactivation of the lemA gene appeared to have rendered the mutant suppressive to B728aN. Neither diminished fitness of the lemA mutant nor its suppressiveness to related strains had been recognized from experiments conducted in controlled environments.