Arabidopsis phospholipase Dα1 and Dδ oppositely modulate EDS1- and SA-independent basal resistance against adapted powdery mildew.

Plants use a tightly regulated immune system to fight off various pathogens. Phospholipase D (PLD) and its product, phosphatidic acid, have been shown to influence plant immunity; however, the underlying mechanisms remain unclear. Here, we show that the Arabidopsis mutants pldα1 and pldδ, respectively, exhibited enhanced resistance and enhanced susceptibility to both well-adapted and poorly adapted powdery mildew pathogens, and a virulent oomycete pathogen, indicating that PLDα1 negatively while PLDδ positively modulates post-penetration resistance. The pldα1δ double mutant showed a similar infection phenotype to pldα1, genetically placing PLDα1 downstream of PLDδ. Detailed genetic analyses of pldδ with mutations in genes for salicylic acid (SA) synthesis (SID2) and/or signaling (EDS1 and PAD4), measurement of SA and jasmonic acid (JA) levels, and expression of their respective reporter genes indicate that PLDδ contributes to basal resistance independent of EDS1/PAD4, SA, and JAsignaling. Interestingly, while PLDα1-enhanced green fluorescent protein (eGFP) was mainly found in the tonoplast before and after haustorium invasion, PLDδ-eGFP's focal accumulation to the plasma membrane around the fungal penetration site appeared to be suppressed by adapted powdery mildew. Together, our results demonstrate that PLDα1 and PLDδ oppositely modulate basal, post-penetration resistance against powdery mildew through a non-canonical mechanism that is independent of EDS1/PAD4, SA, and JA.

Intraspecific genetic variations, fitness cost and benefit of RPW8, a disease resistance locus in Arabidopsis thaliana.

The RPW8 locus of Arabidopsis thaliana confers broad-spectrum resistance to powdery mildew pathogens. In many A. thaliana accessions, this locus contains two homologous genes, RPW8.1 and RPW8.2. In some susceptible accessions, however, these two genes are replaced by HR4, a homolog of RPW8.1. Here, we show that RPW8.2 from A. lyrata conferred powdery mildew resistance in A. thaliana, suggesting that RPW8.2 might have gained the resistance function before the speciation of A. thaliana and A. lyrata. To investigate how RPW8 has been maintained in A. thaliana, we examined the nucleotide sequence polymorphisms in RPW8 from 51 A. thaliana accessions, related disease reaction phenotypes to the evolutionary history of RPW8.1 and RPW8.2, and identified mutations that confer phenotypic variations. The average nucleotide diversities were high at RPW8.1 and RPW8.2, showing no sign of selective sweep. Moreover, we found that expression of RPW8 incurs fitness benefits and costs on A. thaliana in the presence and absence of the pathogens, respectively. Our results suggest that polymorphisms at the RPW8 locus in A. thaliana may have been maintained by complex selective forces, including those from the fitness benefits and costs both associated with RPW8.