Evidence that the BONZAI1/COPINE1 protein is a calcium- and pathogen-responsive defense suppressor

Evidence that the BONZAI1/COPINE1 protein is a calcium- and pathogen-responsive defense suppressor Copines are calcium-responsive, phospholipid-binding proteins involved in cellular signaling. The Arabidopsis BONZAI1/COPINE1 (BON1/CPN1) gene is a suppressor of defense responses controlled by the disease resistance (R) gene homolog SNC1. The BON1/CPN1 null mutant cpn1-1 has a recessive, temperature- and humidity-dependent, lesion mimic phenotype that includes activation of Pathogenesis-Related (PR) gene expression. Here, we demonstrated that the accumulation of BON1/CPN1 protein in wild-type plants was up-regulated by bacterial pathogen inoculation and by the activation of defense signaling responses controlled by two R genes, SNC1 and RPS2. Interestingly, however, over-accumulation of BON1/CPN1 in two BON1/CPN1 promoter T-DNA insertion mutants did not affect resistance to a bacterial pathogen. Promoter deletion analysis identified a 280 bp segment of the BON1/CPN1 promoter as being required for pathogen-induced gene expression; the same promoter region was also required for calcium ionophore-induced gene expression. Leaf infiltration with calcium ionophore triggered high-level PR gene expression specifically in cpn1-1 plants grown under permissive conditions, while co-infiltration of the calcium chelator EGTA attenuated this effect. These results explain the conditional nature of the cpn1-1 phenotype and are consistent with BON1/CPN1 being a calcium- and pathogen-responsive plant defense suppressor. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Plant Molecular Biology Springer Journals

Evidence that the BONZAI1/COPINE1 protein is a calcium- and pathogen-responsive defense suppressor

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Publisher
Springer Netherlands
Copyright
Copyright © 2008 by Springer Science+Business Media B.V.
Subject
Life Sciences; Plant Pathology; Biochemistry, general; Plant Sciences
ISSN
0167-4412
eISSN
1573-5028
D.O.I.
10.1007/s11103-008-9413-6
Publisher site
See Article on Publisher Site

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