Abstract:In this study, the chitosan oligosaccharide (COS) induced resistance to Pst DC3000 was investigated in SPINDLY deficient Arabidopsis mutant spy3. From multilevel indices, including phenotype data, the disease index, the bacterial numbers in infected leaves and the expression of Pst DC3000 marker genes. The function of SPINDLY in COS induced resistance was systematically investigated. The results showed that: (1) spy3 mutant was more susceptible to Pst DC3000 infection than wild type. (2) Compared with the Mock+Pst group, COS pretreatment significantly relieved the leaf symptoms, inhibited the proliferation of Pst DC3000, and reduced the disease index. (3) SA and JAmediated pathway related genes and the contents of SA and JA were upregulated significantly in COS pretreated spy3 plants. (4) The effect of COS induced resistance in spy3 has no significant difference compared with wild type. The results suggested the essential role of SPY in plant innate immunity. However, COS still effectively induce the disease resistance in spy3.