Skip Navigation


Plant and Cell Physiology Advance Access originally published online on January 23, 2007
Plant and Cell Physiology 2007 48(3):414-423; doi:10.1093/pcp/pcm011
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
48/3/414    most recent
pcm011v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (3)
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Takabatake, R.
Right arrow Articles by Ohashi, Y.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Takabatake, R.
Right arrow Articles by Ohashi, Y.
Agricola
Right arrow Articles by Takabatake, R.
Right arrow Articles by Ohashi, Y.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© The Author 2007. Published by Oxford University Press on behalf of Japanese Society of Plant Physiologists. All rights reserved. For permissions, please email: journals.permissions@oxfordjournals.org

Pathogen-Induced Calmodulin Isoforms in Basal Resistance Against Bacterial and Fungal Pathogens in Tobacco

Reona Takabatake1,4, Eri Karita1,2,4, Shigemi Seo1, Ichiro Mitsuhara1, Kazuyuki Kuchitsu2,3 and Yuko Ohashi1,*

1Plant–Microbe Interaction Research, National Institute of Agrobiological Sciences, Tsukuba, Ibaraki, 305-8602 Japan
2Department of Applied Biological Sciences, Tokyo University of Science, 2641 Yamazaki, Noda Chiba, 278-8510 Japan
3Genome and Drug Research Center, Tokyo University of Science, 2641 Yamazaki, Noda Chiba, 278-8510 Japan

*Corresponding author: E-mail, yohashi{at}affrc.go.jp; Fax, + 81-29-8387469.


  Abstract

Thirteen tobacco calmodulin (CaM) genes fall into three distinct amino acid homology types. Wound-inducible type I isoforms NtCaM1 and 2 were moderately induced by tobacco mosaic virus (TMV)-mediated hypersensitive reaction, and the type III isoform NtCaM13 was highly induced, while the type II isoforms NtCaM3–NtCaM12 showed little response. Type I and III knockdown tobacco lines were generated using inverted repeat sequences from NtCaM1 and 13, respectively, to evaluate the contribution of pathogen-induced calmodulins (CaMs) to disease resistance. After specific reduction of type I and III CaM gene expression was confirmed in both transgenic lines, we analyzed the response to TMV infection, and found that TMV susceptibility was slightly enhanced in type III CaM knockdown lines compared with the control line. Resistance to a compatible strain of the bacterial pathogen Ralstonia solanacearum, and fungal pathogens Rhizoctonia solani and Pythium aphanidermatum was significantly lower in type III but not in type I CaM knockdown plants. Expression of jasmonic acid (JA)- and/or ethylene-inducible basic PR genes was not affected in these lines, suggesting that type III CaM isoforms are probably involved in basal defense against necrotrophic pathogens in a manner that is independent of JA and ethylene signaling.

Keywords: Basal defense - Calmodulin - Multigene family - Tobacco - Virulent pathogen

Abbreviations: CaM, calmodulin; d.p.i., days post-inoculation; HR, hypersensitive reaction; IR, inverted repeat; JA, jasmonic acid; PR, pathogenesis-related; RT–PCR, reverse transcription–PCR; TMV, tobacco mosaic virus.

4These authors contributed equally to this work.

(Received December 8, 2006; Accepted January 16, 2007)
Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?




Disclaimer:
Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.