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Characterization of a Novel, Defense-Related Arabidopsis Mutant, cir1, Isolated By Luciferase Imaging

June 2002 , Volume 15 , Number  6
Pages  557 - 566

Shane L. Murray , Catherine Thomson , Andrea Chini , Nick D. Read , and Gary J. Loake

Institute of Cell & Molecular Biology, University of Edinburgh, Daniel Rutherford Building, King's Buildings', Edinburgh EH9 3JH Scotland, U.K.

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Accepted 8 January 2002.

In order to identify components of the defense signaling network engaged following attempted pathogen invasion, we generated a novel PR-1luciferase (LUC) transgenic line that was deployed in an imaging-based screen to uncover defense-related mutants. The recessive mutant designated cir1 exhibited constitutive expression of salicylic acid (SA), jasmonic acid (JA)/ethylene, and reactive oxygen intermediate-dependent genes. Moreover, this mutation conferred resistance against the bacterial pathogen Pseudomonas syringae pv. tomato DC3000 and a virulent oomycete pathogen Peronospora parasitica Noco2. Epistasis analyses were undertaken between cir1 and mutants that disrupt the SA (npr1, nahG), JA (jar1), and ethylene (ET) (ein2) signaling pathways. While resistance against both P. syringae pv. tomato DC3000 and Peronospora parasitica Noco2 was partially reduced by npr1, resistance against both of these pathogens was lost in an nahG genetic background. Hence, cir1-mediated resistance is established via NPR1-dependent and -independent signaling pathways and SA accumulation is essential for the function of both pathways. While jar1 and ein2 reduced resistance against P. syringae pv. tomato DC3000, these mutations appeared not to impact cir1-mediated resistance against Peronospora parasitica Noco2. Thus, JA and ET sensitivity are required for cir1-mediated resistance against P. syringae pv. tomato DC3000 but not Peronospora parasitica Noco2. Therefore, the cir1 mutation may define a negative regulator of disease resistance that operates upstream of SA, JA, and ET accumulation.

Additional keywords: systemic acquired resistance .

© 2002 The American Phytopathological Society