The lower cell density of leaf parenchyma in the Arabidopsis thaliana mutant lcd1-1 is associated with increased sensitivity to ozone and virulent Pseudomonas syringae.
Under optimal growth conditions (120 micro mol photons m-2 sec-1 photosynthetically active radiation (PAR), 16-h photoperiod), the recessive ozone-sensitive Arabidopsis thaliana L. Heynh. mutant lcd1-1 exhibits a pale phenotype compared to the wild type. Confocal and multiphoton microscopy revealed that the paleness of lcd1-1 is because of a lower cell density in the leaf palisade parenchyma, resulting in decreased chlorophyll content. When exposed to ozone, lcd1-1 leaves become paler and contain an increased amount of the lipid peroxidation product malondialdehyde compared to the wild type, suggesting that lcd1-1 suffers from elevated levels of reactive oxygen species (ROS) generated in the apoplast. Infection of leaves with virulent Pseudomonas syringae reveals higher bacterial growth as well as lower pathogenesis-related protein 1 ( PR-1) and PR-5 expression in lcd1-1 than in the wild type. When the wild type and lcd1-1 are exposed to short-term high-light stress, leaves do not bleach in lcd1-1 and potential activities of photosystems I (PSI) and II (PSII) decrease to a similar extent in both the genotypes, indicating that the photosynthetic apparatus is not affected by lcd1-1 mutation. The LCD1 gene, found to contain a nonsense mutation in the mutant, has been identified. It is located at the bottom of chromosome 2 of the Arabidopsis genome. However, the function of the protein encoded by LCD1 is not yet known. We hypothesize that LCD1 plays a role in normal leaf development, and that the increased sensitivity to ozone and virulent P. syringae is a secondary effect that presumably results from the lower-cell-density phenotype in lcd1-1.[1]References
- The lower cell density of leaf parenchyma in the Arabidopsis thaliana mutant lcd1-1 is associated with increased sensitivity to ozone and virulent Pseudomonas syringae. Barth, C., Conklin, P.L. Plant J. (2003) [Pubmed]
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