Abstract
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.
Highlights
Many fungal and oomycete pathogens penetrate the plant cell wall and extract nutrients from host cells by a similar feeding structure called the haustorium
The ‘edr’ phenotype of pldα1δ led us to speculate that PLDα1 may act genetically downstream of PLDδ to modulate plant immunity negatively.Visual scoring of fungal mass on the leaf surface at 12 dpi and quantification of fungal spore production showed that the level of the ‘eds’ of pldδ was almost comparable with that of Col-nahG, a Col-0 transgenic line defective in salicylic acid (SA) signaling due to conversion of SA to catechol by the bacterial SA
We collected genetic evidence to demonstrate that Arabidopsis PLDα1 and PLDδ oppositely modulate basal, post-penetration resistance against powdery mildew,and oomycete pathogens via an ENHANCED DISEASE SUSCEPTIBILITY 1 (EDS1)/PHYTOALEXIN-DEFICIENT 4 (PAD4), SA, and jasmonic acid (JA)-independent pathway
Summary
Many fungal and oomycete pathogens penetrate the plant cell wall and extract nutrients from host cells by a similar feeding structure called the haustorium. One involves focal exocytosis of antimicrobial materials mediated by PENETRATION1 (PEN1), a syntaxin, and its SNARE partners (Collins et al, 2003; Kwon et al, 2008); the other engages the production of glucosinolates by PEN2 myrosinase and subsequent transport of such antifungal chemicals by the PEN3 ATP-binding cassette transporter (Lipka et al, 2005; Stein et al, 2006; Bednarek et al, 2009) Both mechanisms are probably activated upon recognition of conserved pathogen-associated molecular patterns (PAMPs) by cell surface pattern recognition receptors (PRRs), and may be part of PAMP-triggered immunity (PTI) (Jones and Dangl, 2006; Hückelhoven and Panstruga, 2011). While characterized TIRNB-LRRs require the nucleocytoplasmic lipase-like protein ENHANCED DISEASE SUSCEPTIBILITY 1 (EDS1) for signal transduction, most CC-NB-LRRs engage the plasma membrane (PM)-anchored integrin-like protein NONRACE-SPECIFIC DISEASE RESISTANCE 1 (NDR1) for signaling (Cui et al, 2015)
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