Biocontrol of bacterial soft rot of calla lily by elicitor HarpinXoo and N-acyl homoserine lactonase (AttM) |
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Authors: | Fan Jiaqin Qian Guoliang Yang Xue Gu Chunyan Kang Yuejing Ma Yao Hu Baishi Liu Fengquan |
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Institution: | (1) Department of Plant Pathology, College of Plant Protection, Nanjing Agricultural University, 210095 Nanjing, China;(2) Key Laboratory of Monitoring and Management of Crop Diseases and Pest Insects, Ministry of Agriculture, 210095 Nanjing, China; |
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Abstract: | Bacterial soft rot caused by Pectobacterium carotovorum subsp. carotovorum is a serious plant disease in Zantedeschia spp. (also called calla lily). In this study, two independent genes (a N-acyl homoserine lactonase gene attM from Agrobacterium tumefaciens and a hypersensitive response and pathogenicity gene hrf1 from Xanthomonas oryzae pv. oryzae), transcribed by a strong and constitutive Escherichia coli promoter P
lpp
, respectively, were cloned into plasmid pUC19, and was transformed into E. coli, creating strain JM109/pPHA. The result of sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS–PAGE) assay showed
that both genes (hrf1 and attM) were successfully expressed in one plasmid system in strain JM109/pPHA. The expressed HarpinXoo (Hrf1) and AttM protein had the ability of inducing hypersensitive response (HR) in nonhost tobacco and degrading the N-acyl homoserine lactones (AHLs) produced by P. carotovorum subsp. carotovorum, respectively, whereas HarpinXoo and AttM protein did not seem to interfere with the normal growth of this pathogen. In planta, strain JM109/pPHA could significantly
reduce the soft rot disease severity on dormant tubers (control efficiency: 92.8%) or potted plants (control efficiency: 92.4%)
of calla lily. We have first demonstrated the both biocontrol effects of HarpinXoo and AttM proteins (also described as Quorum interference) on the bacterial soft rot disease of calla lily, caused by P. carotovorum subsp. carotovorum. This work provided a potential way to control this serious plant disease. |
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