Involvement of specific calmodulin isoforms in salicylic acid-independent activation of plant disease resistance responses

The Ca2+ signal is essential for the activation of plant defense responses, but downstream components of the signaling pathway are still poorly defined. Here we demonstrate that specific calmodulin (CaM) isoforms are activated by infection or pathogen-derived elicitors and participate in Ca2+-mediated induction of plant disease resistance responses. Soybean CaM (SCaM)-4 and SCaM-5 genes, which encode for divergent CaM isoforms, were induced within 30 min by a fungal elicitor or pathogen, whereas other SCaM genes encoding highly conserved CaM isoforms did not show such response, This pathogen-triggered induction of these genes specifically depended on the increase of intracellular Ca2+ level. Constitutive expression of SCaM-4 and SCaM-5 in transgenic tobacco plants triggered spontaneous induction of lesions and induces an array of systemic acquired resistance (SAR)-associated genes. Surprisingly, these transgenic plants have normal levels of endogenous salicylic acid (SA), Furthermore, coexpression of nahG gene did not block the induction of SAR-associated genes in these transgenic plants, indicating that SA is not involved in the SAR gene induction mediated by SCaM-4 or SCaM-5. The transgenic plants exhibit enhanced resistance to a wide spectrum of virulent and avirulent pathogens, including bacteria, fungi, and virus. These results suggest that specific CaM isoforms are components of a SA-independent signal transduction chain leading to disease resistance.
Publisher
NATL ACAD SCIENCES
Issue Date
1999-01
Language
ENG
Keywords

SYSTEMIC ACQUIRED-RESISTANCE; PROGRAMMED CELL-DEATH; MICROBE INTERACTIONS; DEFENSE RESPONSES; FUNGAL ELICITORS; TOBACCO; CALCIUM; TRANSCRIPTION; EXPRESSION; GENES

Citation

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, v.96, no.2, pp.766 - 771

ISSN
0027-8424
DOI
10.1073/pnas.96.2.766
URI
http://hdl.handle.net/10203/73620
Appears in Collection
BS-Journal Papers(저널논문)
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