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Malamy J, Hennig J, Klessig DF. Temperature-Dependent Induction of Salicylic Acid and Its Conjugates during the Resistance Response to Tobacco Mosaic Virus Infection. Plant Cell. 1992;4(3):359-366doi: 10.1105/tpc.4.3.359.
Malamy, J., Hennig, J., & Klessig, D. F. (1992). Temperature-Dependent Induction of Salicylic Acid and Its Conjugates during the Resistance Response to Tobacco Mosaic Virus Infection. The Plant cell, 4(3), 359-366. https://doi.org/10.1105/tpc.4.3.359
Malamy, J., et al. "Temperature-Dependent Induction of Salicylic Acid and Its Conjugates during the Resistance Response to Tobacco Mosaic Virus Infection." The Plant cell vol. 4,3 (1992): 359-366. doi: https://doi.org/10.1105/tpc.4.3.359
Malamy J, Hennig J, Klessig DF. Temperature-Dependent Induction of Salicylic Acid and Its Conjugates during the Resistance Response to Tobacco Mosaic Virus Infection. Plant Cell. 1992 Mar;4(3):359-366. doi: 10.1105/tpc.4.3.359. PMID: 12297650; PMCID: PMC160135.
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Plant Cell. 1992 Mar;4(3):359-366. doi: 10.1105/tpc.4.3.359.

Temperature-Dependent Induction of Salicylic Acid and Its Conjugates during the Resistance Response to Tobacco Mosaic Virus Infection.

The Plant cell

J. Malamy, J. Hennig, D. F. Klessig

Affiliations

  1. Waksman Institute, Rutgers, The State University of New Jersey, P.O. Box 759, Piscataway, New Jersey 08855.

PMID: 12297650 PMCID: PMC160135 DOI: 10.1105/tpc.4.3.359

Abstract

Increases in endogenous salicylic acid (SA) levels and induction of several families of pathogenesis-related genes (PR-1 through PR-5) occur during the resistance response of tobacco to tobacco mosaic virus infection. We found that at temperatures that prevent the induction of PR genes and resistance, the increases in SA levels were eliminated. The addition of exogenous SA to infected plants at these temperatures was sufficient to induce the PR genes but not the hypersensitive response. However, when the resistance response was restored by shifting infected plants to permissive temperatures, SA levels increased dramatically and preceded PR-1 gene expression and necrotic lesion formation associated with resistance. SA was also found in a conjugated form whose levels increased in parallel with the free SA levels. The majority of the conjugates appeared to be SA glucosides. The same glucoside was formed when plants were supplied with exogenous SA. These results provide further evidence that endogenous SA signals the induction of certain defense responses and suggests additional complexity in the modulation of this signal.

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