Crosstalk in plant resistance

Japanese plant biologists have provided the first molecular evidence that when plants are in combat with environmental stressors they are less able to battle invading pathogens.

Researchers unearth molecular evidence of an antagonistic relationship between abiotic and biotic stress defenses in plants

Japanese plant biologists have provided the first molecular evidence that when plants are in combat with environmental stressors they are less able to battle invading pathogens.

Survival in the plant world depends on the ability to resist not only disease but also changes in the physical surroundings. A mechanism known as systemic acquired resistance (SAR) is one of the defenses plants use against biotic threats such as bacteria, viruses and fungi. Their reactions to abiotic stressors such as temperature, drought and salinity are governed by a different system that is influenced by the plant hormone abscisic acid (ABA).

These defense mechanisms may suppress each other, resulting in reduced disease resistance during times of physical stress, according to previous research. Now a team of researchers, led by Hideo Nakashita from the RIKEN Advanced Science Institute in Wako, has performed the first detailed examination of antagonistic crosstalk between these systems.

By stimulating both resistance systems in various mutants of the model mustard plant Arabidopsis, the team showed that induction of the ABA-mediated environmental stress response suppressed the induction of the disease-fighting SAR mechanism.

The researchers, including Michiko Yasuda of the RIKEN Advanced Science Institute, replicated an abiotic hazard by treating Arabidopsis plants with salt (1). They found that increasing the salinity level significantly suppressed the chemical induction of SAR-based disease resistance. The inhibition of SAR by this response to environmental stress proved to be ABA dependent.

The team also showed that ABA pre-treated Arabidopsis plants could not combat bacterial infection even if SAR-promoting chemicals were introduced. Anti-pathogen resistance genes failed to be expressed in plants that had been treated with ABA, indicating that this chemical, and hence the abiotic stress response, affects the SAR system at a molecular level. Equally, the team found that the activation of SAR suppressed the expression of ABA-responsive and ABA-biosynthesis genes.

Nakashita and his colleagues propose that a three-sided antagonistic interaction between ABA and two other plant hormones, salicyclic acid (SA) and jasmonic acid (JA), controls the response to external abiotic and biotic stresses (Fig. 1). They note that this antagonistic crosstalk would be useful in nature because reactions to both disease and environmental stress require significant amounts of energy for gene expression and metabolic changes, and plants need to regulate the amount of resources given to each reaction to survive. ”Clarification of the detailed mechanism of the antagonistic interaction would enable us to improve crop protection and agricultural systems in adverse environments,” says Nakashita.

Reference

1. Yasuda, M., Ishikawa, A., Jikumaru, Y., Seki, M., Umezawa, T., Asami, T., Maruyama-Nakashita, A., Kudo, T., Shinozaki, K., Yoshida, S. & Nakashita, H. Antagonistic interaction between systemic acquired resistance and the abscisic acid-mediated abiotic stress response in Arabidopsis. The Plant Cell 20, 1678–1692 (2008).

The corresponding author for this highlight is based at the RIKEN Plant Acquired Immunity Research Unit

Published: 07 Nov 2008

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http://www.rikenresearch.riken.jp/research/566/ Link to article on RIKEN Research http://www.rikenresearch.riken.jp/research/566/image_1803.html Figure 1: Schematic of the three-sided antagonistic signaling network between plant hormones in stress responses. Responses to environmental stresses, diseases and wounds—caused by herbivorous caterpillars, for example—are controlled by abscisic acid (ABA), salicylic acid (SA) and jasmonic acid (JA), respectively.

Reference: 

The Plant Cell 20, 1678–1692 (2008)

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Medicine