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Verticillium dahliae's VdNEP acts both as a plant defence elicitor and a pathogenicity factor in the interaction with Helianthus annuus
The soil-borne fungus Verticillium dahliae Kleb. causes a serious wilt disease in many economic crops worldwide, including sunflower. We investigated the role of V. dahliae's necrosis and ethylene-inducing proteins (VdNEP) in the interaction with sunflower. We inoculated two highly and two weak...
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Published in: | Canadian journal of plant pathology 2011-07, Vol.33 (3), p.375-388 |
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Main Authors: | , , , |
Format: | Article |
Language: | English |
Subjects: | |
Online Access: | Get full text |
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Summary: | The soil-borne fungus Verticillium dahliae Kleb. causes a serious wilt disease in many economic crops worldwide, including sunflower. We investigated the role of V. dahliae's necrosis and ethylene-inducing proteins (VdNEP) in the interaction with sunflower. We inoculated two highly and two weakly aggressive V. dahliae isolates onto moderately resistant and susceptible sunflower hybrids. We also synthesized VdNEP protein in vitro and infiltrated it into sunflower control plants to compare its effects with those of the fungus. VdNEP induced wilting symptoms, i.e. chlorosis, necrosis and vascular discoloration but also triggered host defence responses, i.e. hypersensitive response in Nicotiana benthamiana leaves and sunflower cotyledons. It activated the production of reactive oxygen species and the accumulation of fluorescent compounds in sunflower leaves, as well as pathogenesis-related genes (Ha-PR-3 and Ha-PR-5), two defensin genes (Ha-PDF and Ha-CUA1) and those encoding Ha-ACO, Ha-CHOX, Ha-GST and Ha-SCO. The latter suggested that more than one signalling pathway may be involved in the V. dahliae-sunflower interaction. Two other genes (Ha-PAL and Ha-NML1), related to the salicylic acid pathway, were slightly downregulated by VdNEP, suggesting a possible involvement of VdNEP in affecting sunflower defences. The phenotypic changes induced by VdNEP indicate that this protein acts both as a defence elicitor and a pathogenicity factor. |
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ISSN: | 1715-2992 0706-0661 1715-2992 |
DOI: | 10.1080/07060661.2011.579173 |