Calmodulin-like Proteins from Arabidopsis and Tomato are Involved in Host Defense Against Pseudomonas syringae pv. tomato

Calmodulin-like Proteins from Arabidopsis and Tomato are Involved in Host Defense Against... Complex signal transduction pathways underlie the myriad plant responses to attack by pathogens. Ca2+ is a universal second messenger in eukaryotes that modulates various signal transduction pathways through stimulus-specific changes in its intracellular concentration. Ca2+-binding proteins such as calmodulin (CaM) detect Ca2+ signals and regulate downstream targets as part of a coordinated cellular response to a given stimulus. Here we report the characterization of a tomato gene (APR134) encoding a CaM-related protein that is induced in disease-resistant leaves in response to attack by Pseudomonas syringae pv. tomato. We show that suppression of APR134 gene expression in tomato (Solanum lycopersicum), using virus-induced gene silencing (VIGS), compromises the plant’s immune response. We isolated APR134-like genes from Arabidopsis, termed CML42 and CML43, to investigate whether they serve a functionally similar role. Gene expression analysis revealed that CML43 is rapidly induced in disease-resistant Arabidopsis leaves following inoculation with Pseudomonas syringae pv. tomato. Overexpression of CML43 in Arabidopsis accelerated the hypersensitive response. Recombinant APR134, CML42, and CML43 proteins all bind Ca2+ in vitro. Collectively, our data support a role for CML43, and APR134 as important mediators of Ca2+-dependent signals during the plant immune response to bacterial pathogens. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Plant Molecular Biology Springer Journals

Calmodulin-like Proteins from Arabidopsis and Tomato are Involved in Host Defense Against Pseudomonas syringae pv. tomato

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Publisher
Kluwer Academic Publishers
Copyright
Copyright © 2005 by Springer
Subject
Life Sciences; Biochemistry, general; Plant Sciences; Plant Pathology
ISSN
0167-4412
eISSN
1573-5028
D.O.I.
10.1007/s11103-005-8395-x
Publisher site
See Article on Publisher Site

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