Abstract
R-β-homoserine (RBH) and β-aminobutyric acid (BABA) induce resistance against the oomycete Hyaloperonospora arabidopsidis (Hpa) in Arabidopsis, which is based on priming of multiple defense layers, including early acting penetration resistance at the cell wall. Here, we have examined the molecular basis of RBH- and BABA-primed defense by cell wall papillae against Hpa. Three-dimensional reconstruction of Hpa-induced papillae by confocal microscopy revealed no structural differences between control-, RBH-, and BABA-treated plants after Hpa challenge. However, mutations affecting POWDERY MILDEW RESISTANCE 4 or PLASMODESMATA LOCATED PROTEINs (PDLPs) only impaired BABA-induced penetration resistance and not RBH-induced penetration resistance. Furthermore, PDLP1 over-expression mimicked primed penetration resistance, while the intensity of GFP-tagged PDLP1 at germinating Hpa conidiospores was increased in BABA-primed plants but not RBH-primed plants. Our study reveals new regulatory layers of immune priming by β-amino acids and supports the notion that penetration resistance is a multifaceted defense layer that can be achieved through seperate pathways.