Pathogen-induced calmodulin isoforms in basal resistance against bacterial and fungal pathogens in tobacco.

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.