Incompatible pathogen infection results in enhanced reactive oxygen and cell death responses in transgenic tobacco expressing a hyperactive mutant calmodulin |
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Authors: | Scott A Harding Daniel M Roberts |
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Institution: | (1) Department of Biochemistry, Cellular and Molecular Biology and Center for Legume Research, University of Tennessee, Knoxville, TN 37996, USA, US |
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Abstract: | Transgenic tobacco (Nicotiana tabacum L. cv. Wisconsin 38) lines expressing a mutant calmodulin (VU-3) that hyperactivates NAD kinase exhibit an enhanced elicitor-stimulated
oxidative-burst reaction (S.A. Harding et al., 1997, EMBO J. 16: 1137–1144). VU-3 transgenic tobacco was used in the present
study to investigate the relationship between calmodulin signalling, the production of active oxygen species and cell death
in response to infection with an incompatible pathogen. Following P. syringae pv. syringae 61 infection, suspension cells derived from VU-3 transgenic plants exhibited a stronger oxidative burst (3- to 4-fold higher
primary and secondary burst reactions), greater media alkalinization (3-fold) and more rapid cell death (4-fold greater mortality
at 20 h post infection) than did infected control tobacco cells. Infection of leaf tissues with P. syringae pv. syringae 61 also resulted in an enhanced cell death response compared to control tobacco tissues. This cell death response of VU-3
leaf tissues, but not control leaf tissues, was further enhanced by the presence of 50 μM salicylic acid, suggesting that
this transgenic line is more sensitive to the effects of this agent. Overall, the data support the model that calmodulin signalling
pathways are involved in the plant oxidative burst and contribute to the regulation of cell death in infected plant tissues
undergoing the hypersensitive response.
Received: 6 January 1998 / Accepted: 7 March 1998 |
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Keywords: | : Calcium Calmodulin Hypersensitive response NAD kinase Nicotiana (mutant calmodulin) Oxidative burst |
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