The hnRNP-Q Protein LIF2 Participates in the Plant Immune Response

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.真核生物已演化出复杂的防御通路以对抗入侵病原体。本研究探究了拟南芥（Arabidopsis thaliana）异质核核糖核蛋白-Q（heterogeneous nuclear ribonucleoprotein-Q, hnRNP-Q）LIF2在植物先天免疫应答中的作用。研究表明，拟南芥中LIF2功能丧失会分别改变水杨酸（salicylic acid, SA）依赖型防御标记基因PR1以及茉莉酸（jasmonic acid, JA）依赖型防御标记基因PDF1.2的基础表达水平。尽管lif2-1突变体中参与SA和JA生物合成及信号转导的基因表达也受到影响，但并未检测到SA和JA激素含量的变化。此外，在未受到病原体侵染的情况下，lif2-1突变体中一类防御相关次生代谢物——葡萄糖硫苷（glucosinolates）的组成发生了改变。lif2-1突变体对半营养型病原体丁香假单胞菌（Pseudomonas syringae）以及死体营养型子囊真菌灰葡萄孢（Botrytis cinerea）的敏感性降低。此外，lif2-1 sid2-2双突变体对丁香假单胞菌侵染的敏感性较野生型更低，这表明lif2对病原体的应答不依赖于SA的积累。综上，本研究数据表明，lif2-1呈现基础防御启动状态，这一状态由基因表达的复杂失调所导致，进而使其对多种侵染策略的病原体的抗性增强。因此，LIF2可能作为细胞自主免疫的负调控因子发挥作用。与其人类同源蛋白NSAP1/SYNCRIP（一种同时参与细胞进程与病毒生命周期的反式作用因子）类似，LIF2可能调控发育与防御程序间的冲突性调控方向，这表明真核生物中存在生长与防御通路之间保守的进化权衡机制。