Abstract

The ability of the plants to detect diverse stress conditions and initiate cellular responses is vital to their survival in a constantly changing environment. General regulatory molecules often play crucial roles in controlling a multitude of cellular processes throughout the life span of an organism. GCN2 (general control nonderepressible 2) is a serine/threonine-protein kinase that acts as a global translational regulator in all eukaryotes from yeast to mammals to plants. GCN2 plays universal roles in mitigating cellular stresses by directly binding with uncharged tRNAs and phosphorylating its target, eukaryotic initiation factor 2 alpha (eIF2α). Here, we demonstrate that Arabidopsis thaliana GCN2 (AtGCN2) serves as a general regulator of salicylic acid- and jasmonic acid-mediated immune responses triggered upon infection with biotrophic and necrotrophic pathogens. Intriguingly, we found examples of both positive and negative influence of AtGCN2 on plant immunity at different developmental stages. This effect is consistent with the variable amount of abscisic acid accumulation in plants lacking functional AtGCN2 at early stages of development. Finally, we illustrate that AtGCN2 positively contributes to water loss and might also be involved in the epidermis-mediated defense responses.

Highlights

  • The lifestyles of plant pathogens vary considerably ranging from biotrophy to necrotrophy

  • Plants lacking functional Arabidopsis thaliana GCN2 (AtGCN2) exhibit enhanced disease resistance towards a necrotrophic pathogen: Resistance against necrotrophic pathogens is primarily mediated by the stimulation of the JA signaling pathway

  • Given that AtGCN2-mediated phosphorylation of eIF2α is activated by application of methyl jasmonate as well as by mechanical wounding, a JA inducing treatment (Lageix et al, 2008), we hypothesized that AtGCN2 might participate in immune responses against necrotrophic pathogens

Read more

Summary

Introduction

The lifestyles of plant pathogens vary considerably ranging from biotrophy to necrotrophy. Biotrophs establish intimate associations with the plant and require living host cells to complete their infection cycle (Glazebrook, 2005; Spoel et al, 2007). Biotrophs acquire nutrients from the host cell, while residing and growing mainly in the extracellular matrix termed as apoplast. Through their virulent activities, the pathogens establish a nutrient sink at the infection site in such a way that the host is disadvantaged but not killed (Glazebrook, 2005; Spoel et al, 2007).

Results
Discussion
Conclusion
Full Text
Published version (Free)

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