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 define d. Here we demonstrate that specific calmodulin (CaM) isoforms are activate d by infection or pathogen-derived elicitors and participate in Ca2+-mediat ed induction of plant disease resistance responses. Soybean CaM (SCaM)-4 an d SCaM-5 genes, which encode for divergent CaM isoforms, were induced withi n 30 min by a fungal elicitor or pathogen, whereas other SCaM genes encodin g highly conserved CaM isoforms did not show such response, This pathogen-t riggered induction of these genes specifically depended on the increase of intracellular Ca2+ level. Constitutive expression of SCaM-4 and SCaM-5 in t ransgenic tobacco plants triggered spontaneous induction of lesions and ind uces an array of systemic acquired resistance (SAR)-associated genes. Surpr isingly, these transgenic plants have normal levels of endogenous salicylic acid (SA), Furthermore, coexpression of nahG gene did not block the induct ion 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 virule nt and avirulent pathogens, including bacteria, fungi, and virus. These res ults suggest that specific CaM isoforms are components of a SA-independent signal transduction chain leading to disease resistance.