Skip to main content
padlock icon - secure page this page is secure

Free Content Lesion mimic mutants of rice with alterations in early signaling events of defense

Download Article:

The full text article is temporarily unavailable.

We apologise for the inconvenience. Please try again later.


We screened 93 lesion mimic mutants of rice for resistance to the blast fungus, Magnaporthe grisea, and found eight mutants that exhibited significant resistance to the fungus. We called these mutants cdr (cell death and resistance) and further analyzed three of them. Two mutations, cdr1 and cdr2, were recessive and one, Cdr3, was dominant. Many small brownish lesions developed over the entire leaf of the mutants 20–50 days after sowing. TUNEL staining revealed that DNA fragmentation occurred in leaf blade cells of the homozygous Cdr3 mutants. Autofluorescence and callose deposition were visible in leaf cells of these three mutants. Activation of two defense-related genes, PBZ1 and PR1, was observed in the leaves of the mutants; high expression of PBZ1 was correlated with the lesion formation in the three mutants, whereas PR1 was constitutively expressed in the cdr2 and Cdr3 mutants irrespective of the lesion formation. Levels of momilactone A, a major phytoalexin of rice, in these mutants were increased approximately 100–400-fold relative to the wild-type levels. Suspension-cultured cells of the cdr1 and cdr2 but not Cdr3 produced higher levels of H2O2 than the wild type when treated with calyculin A, an inhibitor of protein phosphatase 1. These results suggest that biochemical lesions of cdr1 and cdr2 lie in the early signaling steps leading to activation of the NADPH oxidase and that type-1 protein phosphatase is operative in protein dephosphorylation involved in NADPH oxidase activation.
No References
No Citations
No Supplementary Data
No Article Media
No Metrics

Document Type: Research Article

Publication date: March 1, 1999

  • Access Key
  • Free content
  • Partial Free content
  • New content
  • Open access content
  • Partial Open access content
  • Subscribed content
  • Partial Subscribed content
  • Free trial content
Cookie Policy
Cookie Policy
Ingenta Connect website makes use of cookies so as to keep track of data that you have filled in. I am Happy with this Find out more