| Populus bacterial canker disease (Lonsdalea quercina subsp. populi) has been a serious threat to the development of poplar industry since 2005. There is no economical and effective control measure at the moment. Utilization of resistance of variety can be an alternative way for disease control. In order to provide the experimental basis for explaining the defense response mechanism of poplar’s resistance to canker disease, ten varieties of one year old poplar seedling was inoculated artificially with canker pathogen indoors and in the field, to screen the superior resistance varieties of poplar to bacterial canker. Defense enzyme activities (POD, SOD and PAL) were compared from different resistance varieties of poplars (P.×euramericana cv.74/76’ and’Robusta’) which was inoculated with L.quercina for 0 h-120 h, and endogenous hormone (SA, JA, ABA. GA,IAA) content were investigated of different resistant varieties (’Populus tomentosa’,’Zhonghe 1’,’Robuta’and 74/76’) after inoculation for 9 days. Quantitative real-time PCR was used to detect the differential expression of seventeen genes related to SA and J A signal transduction in "Robuta" after inoculated with canker pathogern for 1d,3d,6d and 9d, and analyzed twelve genes selected from above in the resistant and susceptible varieties (’Populus tomentosa’,’Zhonghe 1’). The main results are as follows:Survey from inoculation indoor and outdoor showed that ’Populus tomentosa’was high resistance, and 74/76’ showed medium resistance, whereas 313’, Tianyan’, and ’599’, showed high susceptible. Resistance of ’Zhonghel’,’Robuta’, 01’, Zhonglin 2001’, ’N-179’ behave differently indoor and outdoor.The results indicated that the inoculation of pathogen to poplar increase POD, SOD and PAL activity both in the resistant and susceptible varieties, and present the tendence that increased first and decreased later over inoculation time. In addition, the periods of POD, SOD and PAL activity increased to peak in susceptible varieties were earlier than that of disease-resistant varieties. However, the activity peak of three enzymes from resistant varieties were higher than that of susceptible varieties.The results showed that canker pathogen decrease the content of endogenous IAA from ’74/76’ and ’Robuta’, however, endogenous IAA from P. tomentosa’increased significantly,and the content of IAA has no any significant change in’Zhonghel’. The content of endogenous ABA from’Zhonghe 1’and 74/76’ was not significantly reduced. The increased rate of ABA from’Robuta’was higher than that of ’Zhonghe 1’. The content of endogenous GA from’P. tomentosa’and 74/76’ was significantly reduced, especially in 74/76’,; whereas GA from ’Robuta’was as doubled higher as the control group. The content of endogenous SA were significantly increased in’Robuta’ and in 74/76’, poplar, while there was no any significant change in that of’Zhonghe 1’and ’P. tomentosa’. The increased content of endogenous JA from 74/76’, was higher than that of’Robuta’and’P. tomentosa’whereas endogenous JA from’Zhonghe 1’decreased significantly. There is no significant correlation between the endogenous hormone content and the resistance of five poplar varieties.Inoculated with L. quercina on’Robuta’, gene of PR1-1, PR1-2, PR1-3, PR1-4was up-regulated in different degree within 9d. Canker pathogen can increase the expression of TGA2 and MYC2-1 but make NPR1-3 and MYC2-2 down-regulated. The expression of JAZ2, COI1-1, NPR1-1, NPR1-2 and MYC2-3 decreased first and then up-regulated. The expression of TGA1ã€JAZ1〠COI1-2 did not show significant difference after the inoculation.In resistant variety, the expression of PR1-1, PR1-2, NPR1-1, NPR1-2, TGA1, TGA2, MYC2-1 and MYC2-2 was higher than that in susceptible one, especially the genes PR1-1, MYC2-1 and MYC2-2. While, JAZ1, COI1-1 and COI1-2 were expressed lower in resistant variety than that in susceptible one. The expression of JAZ2 didn’t show significant difference after the inoculation. It suggests that the reason for resistance against canker disease in’Populus tomentosa’is related to the up-regulated expression of PR1-1, PR1-2, NPR1-1, NPR1-2, TGA1, TGA2, MYC2-1, MYC2-2 and the down-regulated expression of JAZ1, COI1-1 and COI1-2, which can start the SA and JA signal transduction to defend the disease. |