Location: Natural Products Utilization ResearchTitle: Priming of jasmonate-mediated anti-herbivore defense responses in rice by silicon Author
|Pan, Zhiqiang - Peter|
|Xie, Jie Feng|
|Cai, Kun Zheng|
|Luo, Shi Ming|
|Zeng, Ren Sen|
Submitted to: Proceedings of the National Academy of Sciences
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 8/6/2013
Publication Date: 9/3/2013
Citation: Ye, M., Song, Y., Long, J., Zhu-Salzman, K., Baerson, S.R., Pan, Z., Xie, J., Cai, K., Luo, S., Zeng, R. 2013. Priming of jasmonate-mediated anti-herbivore defense responses in rice by silicon. Proceedings of the National Academy of Sciences. p.E3631-E3639. Interpretive Summary: For many years, treatment of plants with the mineral silicon has been known to improve their ability to withstand the effects of a wide variety of stresses, although silicon is not considered essential or necessarily beneficial for the normal growth and development of non-stressed plants. This phenomenon has been observed for both so-called abiotic stresses such as tolerance to cold and drought, as well as biotic stresses such as insect attack and infection by pathogenic microorganisms. While the role of silicon in enhancing resistance to various stresses has been unequivocally established, details surrounding the underlying mechanism for how its effects are mediated remain largely unknown. In this study we have established a link between the stress-associated plant hormone jasmonic acid (JA), which regulates plant responses to diverse stresses, and the effects of silicon. Attack of rice plants by the destructive leaf folder (LF) insect herbivore was used as the focus of this work, and silicon treatment was shown to significantly reduce the damage to rice plants caused by this herbivore. Mutant plant lines unable to produce or perceive JA derived no benefit from silicon during LF attack, and the development of specialized silicon-bearing cells in leaves was also found to be compromised in these mutant lines. Additionally, treatment with silicon was found to enhance the protective responses normally regulated by JA, including the increased expression of genes associated with plant defense mechanisms. Thus silicon appears to have become integrated into the defensive arsenal associated with the hormone JA in certain species such as rice, and actually enhances the ability of JA to mount effective responses against attack by herbacious insects.
Technical Abstract: While the function of silicon (Si) in plant physiology has long been debated, its beneficial effects on plant resistance against abiotic and biotic stresses, ¬including insect herbivory, have been well-documented. In addition, the jasmonate (JA) signaling pathway plays a crucial role in mediating anti-herbivore defense responses in plants, however potential interactions between JA and Si in response to insect attack have not been directly examined. To explore the role JA may play in Si-enhanced resistance, we silenced allene oxide synthase (OsAOS, JA biosynthesis) and CORONATINE INSENSITIVE1 (OsCOI1, JA perception) in transgenic rice plants via RNAi, and examined resulting changes in Si accumulation and various defense responses against the chewing insect leaf folder (LF). Si pre-treatment increased rice resistance against LF larvae in wild-type (WT) plants but not in OsAOS and OsCOI1 RNAi lines. Upon LF attack, WT plants subjected to Si pre-treatment exhibited enhanced defense responses relative to untreated controls, including higher JA accumulation levels, increased levels of transcripts encoding defense marker genes, and elevated activities of peroxidase, polyphenol oxidase and trypsin protease inhibitor. Additionally, reduced Si deposition and Si cell expansion was observed in leaves of OsAOS and OsCOI1 RNAi plants in comparison to WT plants, as well as reduced steady-state transcript levels of Si transporters OsLsi1, OsLsi2 and OsLsi6 following LF attack in Si pre-treated plants. These results suggest a strong interaction between Si and JA in defense against insect herbivores, involving priming of JA-mediated defense responses by Si, and the promotion of Si accumulation by JA.