|Lawrence, Christopher - VIRGINIA TECH|
|Schardl, Christopher - UNI OF KENTUCKY|
Submitted to: Physiological and Molecular Plant Pathology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: February 25, 2005
Publication Date: June 23, 2005
Citation: Funnell, D., Lawrence, C., Pedersen, J.F., Schardl, C. 2005. Expression of the tobacco beta-1,3 glucanase gene Pr-2d during induction of SAR with Peronospora tabacina. Physiological and Molecular Plant Pathology. Vol 65/6 pp 285-296. Interpretive Summary: Systemic acquired resistance (SAR) is a plant phenomenon in which an initial infection can result in immunity to a secondary infection. It is known that SAR can be triggered in susceptible tobacco with the pathogen, Peronospora tabacina. SAR is associated with the certain plant proteins, which may contribute to resistance. We investigated regulation of genes for these proteins following SAR induction with P. tabacina and demonstrated that increased activity of at least two SAR genes were correlated with resistance to secondary infection.
Technical Abstract: Systemic acquired resistance (SAR) is induced following inoculation of Peronospora tabacina sporangia into the stems of Nicotiana tabacum plants highly susceptible to the pathogen. Previous results have shown that accumulation of acidic '-1,3-glucanases (PR-2’s) following induction of SAR by P. tabacina may contribute to resistance to P. tabacina. We showed that up-regulation of the PR-2 gene, PR-2d, following stem inoculation with P. tabacina, is associated with SAR. Studies using plants transformed with GUS constructs containing the full length promoter from PR-2d or promoter deletions, provided evidence that a previously characterized regulatory element that is involved in response to salicylic acid, may be involved in regulation of PR-2d following induction of SAR with P. tabacina. This work provides evidence that regulation of PR-2 genes during P. tabacina-induced SAR may be similar to regulation of these genes during infection of N-gene tobacco by TMV or following exogenous application of SA, and provide further support for the role of SA in regulation of genes during P. tabacina-induced SAR.