The hnRNP-Q protein LIF2 participates in the plant immune response.

Clémentine Le Roux,François Perreau,Mathilde Fagard,Stefania Del Prete,Dominique Roby,Stéphanie Boutet-Mercey,Valérie Gaudin,Claudine Balagué,Xiaoyu Zhang

doi:10.1371/journal.pone.0099343

Abstract

Eukaryotes have evolved complex defense pathways to combat invading pathogens. Here, we investigated the role of the Arabidopsis thaliana heterogeneous nuclear ribonucleoprotein (hnRNP-Q) LIF2 in the plant innate immune response. We show that LIF2 loss-of-function in A. thaliana leads to changes in the basal expression of the salicylic acid (SA)- and jasmonic acid (JA)- dependent defense marker genes PR1 and PDF1.2, respectively. Whereas the expression of genes involved in SA and JA biosynthesis and signaling was also affected in the lif2-1 mutant, no change in SA and JA hormonal contents was detected. In addition, the composition of glucosinolates, a class of defense-related secondary metabolites, was altered in the lif2-1 mutant in the absence of pathogen challenge. The lif2-1 mutant exhibited reduced susceptibility to the hemi-biotrophic pathogen Pseudomonas syringae and the necrotrophic ascomycete Botrytis cinerea. Furthermore, the lif2-1 sid2-2 double mutant was less susceptible than the wild type to P. syringae infection, suggesting that the lif2 response to pathogens was independent of SA accumulation. Together, our data suggest that lif2-1 exhibits a basal primed defense state, resulting from complex deregulation of gene expression, which leads to increased resistance to pathogens with various infection strategies. Therefore, LIF2 may function as a suppressor of cell-autonomous immunity. Similar to its human homolog, NSAP1/SYNCRIP, a trans-acting factor involved in both cellular processes and the viral life cycle, LIF2 may regulate the conflicting aspects of development and defense programs, suggesting that a conserved evolutionary trade-off between growth and defense pathways exists in eukaryotes.

Highlights

Living organisms are exposed to various abiotic and biotic stresses and continuously integrate diverse signals to limit the spread of microbial pathogens
Given that the human homolog of LIF2, the NSAP1/SYNCRIP protein, is a trans-acting factor involved in both cellular processes and the viral life cycle [3,4,5], we propose that the conserved heterogeneous nuclear ribonucleoprotein (hnRNP)-Q proteins may have an evolutionary conserved function in regulating the trade-off between growth and defense in eukaryotes
In a previous transcriptome profiling experiment, we showed that genes that were deregulated in the A. thaliana lif2-1 null mutant were greatly enriched in Gene Ontology (GO) terms involved in responses to stress stimuli [12]

Summary

Introduction

Living organisms are exposed to various abiotic and biotic stresses and continuously integrate diverse signals to limit the spread of microbial pathogens. RNAbinding proteins (RBPs), which are involved in various aspects of RNA processing (i.e., mRNA maturation, editing, splicing, and mRNA trafficking), are thought to be key regulators of stress responses in both animals and plants. The heterogeneous nuclear ribonucleoprotein (hnRNP) group of RBPs forms a large family of ancestral modular proteins with a high degree of functional diversification [1] In humans, this group contains 37 members, only a few of which are involved in the stress response. HnRNP-I was shown to interact with the long non-coding RNA RoR to modulate the expression of the tumor suppressor p53 in response to DNA damage and to participate in a surveillance network [6]

Methods

Results

Conclusion