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Calmodulin-like proteins from Arabidopsis and tomato are involved in host defense against Pseudomonas syringae pv. tomato
BTI, Cornell University, USA.
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2005 (English)In: Plant Molecular Biology, ISSN 0167-4412, E-ISSN 1573-5028, Vol. 58, no 6, 887-897 p.Article in journal (Refereed) Published
Abstract [en]

Complex signal transduction pathways underlie the myriad plant responses to attack by pathogens. Ca-2 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.

Place, publisher, year, edition, pages
2005. Vol. 58, no 6, 887-897 p.
Keyword [en]
Arabidopsis, calcium, calmodulin, plant defense response, tomato
National Category
Biochemistry and Molecular Biology
URN: urn:nbn:se:kth:diva-71987DOI: 10.1007/s11103-005-8395-xISI: 000232763000010OAI: diva2:487095
QC 20120306Available from: 2012-01-31 Created: 2012-01-31 Last updated: 2012-03-06Bibliographically approved

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Ekengren, Sophia K.
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