Zhang_2018_J.Exp.Bot_69_3675

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 pldalpha1 and plddelta, respectively, exhibited enhanced resistance and enhanced susceptibility to both well-adapted and poorly adapted powdery mildew pathogens, and a virulent oomycete pathogen, indicating that PLDalpha1 negatively while PLDdelta positively modulates post-penetration resistance. The pldalpha1delta double mutant showed a similar infection phenotype to pldalpha1, genetically placing PLDalpha1 downstream of PLDdelta. Detailed genetic analyses of plddelta 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 PLDdelta contributes to basal resistance independent of EDS1/PAD4, SA, and JAsignaling. Interestingly, while PLDalpha1-enhanced green fluorescent protein (eGFP) was mainly found in the tonoplast before and after haustorium invasion, PLDdelta-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 PLDalpha1 and PLDdelta oppositely modulate basal, post-penetration resistance against powdery mildew through a non-canonical mechanism that is independent of EDS1/PAD4, SA, and JA.