Plant and Cell Physiology Advance Access published online on February 5, 2008
Plant and Cell Physiology, doi:10.1093/pcp/pcn015
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The necrotroph Botrytis cinerea induces a non-host Type II resistance mechanism in Pinus pinaster suspension-cultured cells
Grupo de Bioquímica e Fisiologia Molecular de Plantas, Departamento de Biologia, Universidade do Minho, Campus de Gualtar, 4710-057 Braga, Portugal
Corresponding author: Herlánder Azevedo, Tlf: +351 253604047, Fax: +351 253678980 , Email: hazevedo{at}bio.uminho.pt, Address: Grupo de Bioqu7iacute;mica e Fisiologia Molecular de Plantas, Departamento de Biologia, Universidade do Minho, Campus de Gualtar, 4710-057 Braga, Portugal
| Abstract |
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Models of non-host resistance have failed to account for the pathogenicity of necrotrophic agents. During the interaction of Pinus pinaster (maritime pine) with the non-host necrotrophic pathogen Botrytis cinerea, the generation and scavenging of reactive oxygen species (ROS) and the induction of the hypersensitive response (HR) were analyzed. Elicitation of maritime pine suspended cells with B. cinerea spores resulted in the biphasic induction of reactive oxygen species. The phase I oxidative burst was dependent on calcium influx, while the phase II oxidative burst also depended on NADPH oxidase, protein kinase activity, and de novo transcription and protein synthesis. A decline was observed in catalase (CAT) and superoxide dismutase (SOD) activity, together with the down-regulation of Fe-Sod1, chlCu,Zn-Sod1 and csApx1, suggesting a co-ordinated response towards a decrease in the ROS-scavenging capacity of maritime pine cells during challenging. Following the second oxidative burst, programmed cell death events characteristic of the hypersensitive response were observed. Results suggest the ROS-mediated and cell-breach-independent activation of Type II non-host resistance during the Pinus pinaster-Botrytis cinerea interaction.
Keywords: Botrytis cinerea - necrotrophic fungi - non-host Type II resistance - Pinus pinaster - ROS
(Received July 20, 2007; Accepted January 25, 2008)
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