Journal
MOLECULAR PLANT PATHOLOGY
Volume 7, Issue 6, Pages 579-592Publisher
BLACKWELL PUBLISHING
DOI: 10.1111/j.1364-3703.2006.00363.X
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The function of the cell wall protein extensin has been the subject of much speculation since it was first isolated over 40 years ago. In order to investigate the role of extensins in plant defence, we used the gain-of-function strategy to generate transgenic Arabidopsis plants over-expressing the EXT1 extensin gene. These were infected with the virulent bacterial pathogen Pseudomonas syringae DC3000 and symptom development was monitored. Lesions on the transgenics were on average five-fold smaller than those on the wild-type, did not increase in area over the time period of infection, accumulated a small bacterial load and showed very little chlorosis outside the lesion boundary. By contrast, lesions on the wild-type were large, spread to over 50% of the leaf area, continued to increase in size over the time course of the infection, accumulated a bacterial load 100-fold higher than that found in the transgenics, and showed a large chlorotic area outside the lesion boundary. SEM of lesions showed no evidence of bacteria at the lesion boundary in the extensin-over-expressing transgenics, whereas bacteria were always seen at the lesion boundary on the wild-type. Analysis of transgenics carrying an EXT1-GUS promoter-reporter fusion showed expression of GUS in a ring around the boundary of the lesion. Basal defences and signal transduction pathways involved in plant defence were not perturbed in the transgenics, as shown by the analysis of the expression of PR1 and PDF1.2 genes. These results show that extensin over-expression limits pathogen invasiveness.
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