Abstract

Two important role players in plant defence response are the phytohormones salicylic acid (SA) and jasmonic acid (JA); both of which have been well described in model species such as Arabidopsis thaliana. Several pathogenesis related (PR) genes have previously been used as indicators of the onset of SA and JA signaling in Arabidopsis. This information is lacking in tree genera such as Eucalyptus. The aim of this study was to characterize the transcriptional response of PR genes (EgrPR2, EgrPR3, EgrPR4, EgrPR5, and EgrLOX) identified in Eucalyptus grandis to SA and methyl jasmonate (MeJA) treatment as well as to qualify them as diagnostic for the two signaling pathways. Using the genome sequence of E. grandis, we identified candidate Eucalyptus orthologs EgrPR2, EgrPR3, EgrPR4, EgrPR5, and EgrLOX based on a co-phylogenetic approach. The expression of these genes was investigated after various doses of SA and MeJA (a derivative of JA) treatment as well as at various time points. The transcript levels of EgrPR2 were decreased in response to high concentrations of MeJA whereas the expression of EgrPR3 and EgrLOX declined as the concentrations of SA treatment increased, suggesting an antagonistic relationship between SA and MeJA. Our results support EgrPR2 as potentially diagnostic for SA and EgrPR3, EgrPR4, and EgrLOX as indicators of MeJA signaling. To further validate the diagnostic potential of the PR genes we challenged E. grandis clones with the fungal necrotrophic pathogen Chrysoporthe austroafricana. The tolerant clone showed high induction of EgrPR2 and decreased transcript abundance of EgrPR4. Pre-treatment of the susceptible genotype with 5 mM SA resulted in lesion lengths comparable to the tolerant genotype after artificial inoculation with C. austroafricana. Thus expression profiling of EgrPR2 and EgrPR4 genes could serve as a useful diagnostic approach to determine which of the two signaling pathways are activated against various pathogens in Eucalyptus.

Highlights

  • The defence mechanisms that are employed by plants to deter pathogens have been well-studied in various model organisms such as Arabidopsis thaliana

  • Putative orthologs for the following candidates, EgrPR3, EgrPR4, and EgrLOX2 were profiled as signature defence genes of the jasmonic acid (JA) pathway

  • The putative orthologous signature defence genes identified here provide suitable candidates for further investigation in complementation and functional studies to better understand the role of these genes in E. grandis

Read more

Summary

Introduction

The defence mechanisms that are employed by plants to deter pathogens have been well-studied in various model organisms such as Arabidopsis thaliana. These model systems have created a foundation for understanding general host responses to pathogens. Following the plants perception of an invading pathogen, a plethora of defences responses are activated. The phytohormones SA and JA have been extensively investigated in various pathosystems These studies have shown that biotrophic pathogens are impeded by the activation of the SA pathway whereas necrotrophic pathogens are targeted by induction of JA and ET signaling pathways (Glazebrook, 2005). Each of these signaling cascades has been shown to involve the activation of certain signature defence genes, e.g., Pathogenesis Related (PR) genes, which can be representative of the induction of a pathway (Reymond and Farmer, 1998)

Objectives
Methods
Results
Conclusion
Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.