Characterization of the resistance of calamondin and kumquat to Xanthomonas axonopodis pv. citri

• Main Authors: Po-Sheng Chen, 陳柏昇
• Other Authors: Miin-Huey Lee
• Format: Others
• Language: zh-TW
• Published: 2010
• Online Access: http://ndltd.ncl.edu.tw/handle/68841273841504730613

碩士 === 國立中興大學 === 植物病理學系所 === 98 === Citrus canker caused by Xanthomonas axonopodis pv. citri (Xac) is one of the most severe bacterial disease on citrus. Xac caused erumpent and corky lesion on leaves, stems and fruits. It has long been known that some citrus relatives including calamondin (Citrus madurensis) and kumquat (Fortunella spp.) are highly resistant to Xac compared to commercial cultivars of citrus. My research is focused on the interactions of Xac and resistant varieties, calamondin and oval kumquat (Fortunella margarita). Pathogenicity assays using needle prick inoculation on leaf revealed that Xac induced flatter necrotic lesions and less lesion numbers on calamondin and oval kumquat, but promoted characteristic canker lesions with raised and corky appearance on the susceptible variety, Mexican lime (Citrus aurantifolia). When inoculated by infiltration with 105 CFU/ml of bacterial cells in leaf, Xac propagated at lower rate in both oval kumquat and calamondin compared to Mexican lime and raised and corky symptom was only shown on Mexican lime 7 days post-infiltration (7 DPI). When inoculated with 107 CFU/ml of bacterial cells, Xac propagated at lower rate in oval kumquat compared to Mexican lime or calamondin. Water-soaked or symptomless was observed on infiltrated oval kumquat leaves but raised and corky symptom was shown on Mexican lime and calamondin at 7 DPI. When inoculated with 108 CFU/ml of bacterial cells, the central part of infiltrated area was necrotic on calamondin and oval kumquat leaves and severe raised and corky symptom was shown on Mexican lime at 7 DPI. Xac propagated well and reached to the similar population levels in the three plants in unnecrotic infiltrated areas. Wounded Mexican lime leaf, but not wounded oval kumquat and calamondin leaf, could attract Xac. Biofilm formation analysis showed no difference on Xac biofilm formation on intact leaves of the three plants. Further analysis revealed that the peel, but not leaf, extracts from calamondin or kumquat displayed inhibitory effects to Xac as assayed in culture, implicating the presence of preformed compounds. H2O2 accumulation was observed by 3,3’-diaminobenzidine (DAB) detection in leaves of Xac-infiltrated oval kumquat at early infection stage. Antioxidant enzyme activites were detected in Xac-infected and un-treated leaves including superoxide dismutase (SOD), catalase, glutathione reductase (GR) and glutathione peroxidase (GPx) . The levels of antioxidant enzymes were changeless or slightly increased in Mexican lime and calamondin after Xac infection. In oval kumquat catalase and GR activities decreased after Xac infection. Thus, our results suggest that both preformed and induced defense compounds of kumquat may have an important role in cellular resistance to Xac, while preformed compounds may contribute more than antioxidant enzymes for calamondin on resistence to Xac infection.