title: Involvement of specific calmodulin isoforms in salicylic acid-independent activation of plant disease resistance responses.
abstract: 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.
authors.affiliation: Department of Biochemistry, Plant Molecular Biology and Biotechnology Research Center, Gyeongsang National University, Chinju 660-701, Korea.
authors.forename: W D
authors.initials: WD
authors.lastname: Heo
authors.forename: S H
authors.initials: SH
authors.lastname: Lee
authors.forename: M C
authors.initials: MC
authors.lastname: Kim
authors.forename: J C
authors.initials: JC
authors.lastname: Kim
authors.forename: W S
authors.initials: WS
authors.lastname: Chung
authors.forename: H J
authors.initials: HJ
authors.lastname: Chun
authors.forename: K J
authors.initials: KJ
authors.lastname: Lee
authors.forename: C Y
authors.initials: CY
authors.lastname: Park
authors.forename: H C
authors.initials: HC
authors.lastname: Park
authors.forename: J Y
authors.initials: JY
authors.lastname: Choi
authors.forename: M J
authors.initials: MJ
authors.lastname: Cho
mesh_terms: D002118:Calcium / Q000494:pharmacology*; D002147:Calmodulin / Q000235:genetics*; D005670:Fusarium / Q000472:pathogenicity; D018506:Gene Expression Regulation, Plant / Q000235:genetics*; D017343:Genes, Plant / Q000235:genetics; D007113:Immunity, Innate / Q000235:genetics*; D010641:Phenotype; D010838:Phytophthora / Q000472:pathogenicity; D010935:Plant Diseases; D010940:Plant Proteins / Q000235:genetics; D030821:Plants, Genetically Modified; D010947:Plants, Toxic; D011549:Pseudomonas / Q000472:pathogenicity; D020156:Salicylic Acid / Q000378:metabolism*; D013025:Glycine max / Q000378:metabolism*; D014026:Nicotiana / Q000235:genetics / Q000382:microbiology; D015533:Transcriptional Activation
chemical_list: D002147:Calmodulin; D010940:Plant Proteins; D020156:Salicylic Acid; D002118:Calcium