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Jasmonate-Inducible Genes Are Activated in Rice by Pathogen Attack without a Concomitant Increase in Endogenous
P. Schweizer1, A. Buchala, P. Silverman
1Institut de Biologie Vegetale, University of Fribourg, Rte Albert-Gockel 3, CH-1700 Fribourg, Switzerland (P. Schweizer, A.B., J.-P.M.).
Plant Physiology
|May 1, 1997
Summary
Jasmonic acid (JA) application in rice (Oryza sativa L.) induces defense genes, but pathogen attack doesn't require increased JA levels for this response. JA does not orchestrate localized rice defense against pathogens.
Area of Science:
- Plant Pathology
- Molecular Biology
- Plant Biochemistry
Background:
- The octadecanoid signaling pathway, with jasmonic acid (JA) as a key component, is implicated in plant defense responses.
- Understanding JA's role in rice (Oryza sativa L.) defense against pathogens like Magnaporthe grisea is crucial for crop protection.
Purpose of the Study:
- To investigate the role of the octadecanoid signaling pathway and jasmonic acid (JA) in regulating defense genes in rice upon pathogen attack.
- To compare gene expression patterns following JA treatment versus M. grisea inoculation in rice seedlings.
Main Methods:
- Rice seedlings were treated with JA or inoculated with M. grisea.
- Gene expression patterns were analyzed at mRNA and protein levels.
- The effect of tetcyclacis, a jasmonate biosynthesis inhibitor, on pathogen-induced protein accumulation was assessed.
Main Results:
- JA application induced pathogenesis-related (PR) gene products, but M. grisea infection did not increase (-)-JA levels during PR gene expression.
- Pathogen-induced PR1-like protein accumulation was reduced by tetcyclacis.
- JA and M. grisea elicitors showed additive and negative interactions on specific protein inductions.
Conclusions:
- Accumulation of nonconjugated (-)-JA is not essential for PR gene induction in rice.
- Jasmonic acid (JA) does not appear to direct localized defense responses in pathogen-attacked rice.
- JA is likely part of a broader signaling network and may be required at minimal levels for some PR gene induction.