In nature， plants need to respond to multiple environmental stresses that require the involvement and fine-tuning of different stress signaling pathways. Cross-tolerance， in which plants pre-treated with chitin (a fungal microbe-associated molecular pattern) have improved salt tolerance， was observed in Arabidopsis， but is not well understood. Here， we show a unique link between chitin and salt signaling mediated by the chitin receptor CHITIN ELICITOR RECEPTOR KINASE 1 (CERK1). Transcriptome analysis revealed that salt stress-induced genes are highly correlated with chitin-induced genes， although this was not observed with other microbe-associated molecular patterns (MAMPs) or with other abiotic str... More
In nature， plants need to respond to multiple environmental stresses that require the involvement and fine-tuning of different stress signaling pathways. Cross-tolerance， in which plants pre-treated with chitin (a fungal microbe-associated molecular pattern) have improved salt tolerance， was observed in Arabidopsis， but is not well understood. Here， we show a unique link between chitin and salt signaling mediated by the chitin receptor CHITIN ELICITOR RECEPTOR KINASE 1 (CERK1). Transcriptome analysis revealed that salt stress-induced genes are highly correlated with chitin-induced genes， although this was not observed with other microbe-associated molecular patterns (MAMPs) or with other abiotic stresses. The cerk1 mutant was more susceptible to NaCl than was the wild type. cerk1 plants had an irregular increase of cytosolic calcium ([Ca ] ) after NaCl treatment. Bimolecular fluorescence complementation (BiFC) and co-immunoprecipitation experiments indicated that CERK1 physically interacts with ANNEXIN 1 (ANN1)， which was reported to form a calcium-permeable channel that contributes to the NaCl-induced [Ca ] signal. In turn， ann1 mutants showed elevated chitin-induced rapid responses. In short， molecular components previously shown to function in chitin or salt signaling physically interact and intimately link the downstream responses to fungal attack and salt stress.
