(126 words)The inhibition of elicitor-induced plant defense responses by the protein kinase inhibitors K252a and staurosporine indicates that defense responses require protein phosphorylation.We isolated a cDNA clone encoding lectin receptor-like kinase 1 (NtlecRK1), an elicitorresponsive gene, in tobacco bright yellow (BY-2) cells by a differential display method.

SUMMARY Non‐host resistance is the most general form of disease resistance in plants because it is effective against most phytopathogens. The importance of hypersensitive responses (HRs) in non‐host resistance of Nicotiana species to the oomycete Phytophthora is clear. INF1 elicitin, an elicitor obtained from the late‐blight pathogen Phytophthora infestans, is sufficient to induce a typical HR in Nicotiana species. The molecular mechanisms that underlie the non‐host resistance component of plant defence responses have been investigated using differential‐display polymerase chain reaction (PCR) in a model HR system between INF1 elicitin and tobacco BY‐2 cells. Differential‐display PCR has revealed that Cdc27B is down‐regulated in tobacco BY‐2 cells after treatment with INF1 elicitin. Cdc27B is one of 13 essential components of the anaphase‐promoting complex or cyclosome (APC/C)‐type E3 ubiquitin ligase complex in yeast. This APC/C‐type E3 ubiquitin ligase complex regulates G2‐to‐M phase transition of the cell cycle by proteolytic degradation. In this study, we investigated the roles of this gene, NbCdc27B, in plant defence responses using virus‐induced gene silencing. Suppression of NbCdc27B in Nicotiana benthamiana plants induced defence responses and a gain of resistance to Colletotrichum lagenarium fungus. Elicitin‐induced hypersensitive cell death (HCD) was inhibited mildly in plants silenced with tobacco rattle virus::Cdc27B. Cdc27B could manage the signalling pathways of plant defence responses as a negative regulator without HCD.