The copines are a widely distributed class of calcium-dependent, phospholipid-binding proteins of undetermined biological function. Mutation of the Arabidopsis CPN1 (COPINE 1) gene causes a humidity-sensitive lesion mimic phenotype with increased resistance to a bacterial and an oomyceteous pathogen, constitutive pathogenesis-related gene expression, and an accelerated hypersensitive cell death defense response. Here, we show that the disease resistance phenotype of the cpn1-1 mutant was also temperature sensitive, demonstrate increased CPN1 gene transcript accumulation in wild-type plants under low-humidity conditions, and present a detailed analysis of CPN1 gene transcript accumulation in response to bacterial pathogens. In wild-type plants, CPN1 transcript accumulation was rapidly, locally, and transiently induced by both avirulent and virulent strains of Pseudomonas syringae pv tomato bacteria. However, induction of CPN1 transcript accumulation by avirulent bacteria was much faster and stronger than that induced by virulent bacteria. Bacterial induction of CPN1 transcript accumulation was dependent on a functional type III bacterial protein secretion system. In planta expression of the avrRpt2 avirulence gene was sufficient to trigger rapid CPN1 transcript accumulation. CPN1 transcript accumulation was induced by salicylic acid treatment but was not observed during lesion formation in the lesion mimic mutants lsd1 and lsd5. These results are consistent with CPN1 playing a role in plant disease resistance responses, possibly as a suppressor of defense responses including the hypersensitive cell death defense response. The results also suggest that CPN1 may represent a link between plant disease resistance and plant acclimation to low-humidity and low-temperature conditions.
All Science Journal Classification (ASJC) codes
- Plant Science