Characterization of an <i>Arabidopsis–Phytophthora</i> Pathosystem: resistance requires a functional PAD2 gene and is independent of salicylic acid, ethylene and jasmonic acid signalling

<i>Arabidopsis</i> accessions were screened with isolates of <i>Phytophthora porri</i> originally isolated from other crucifer species. The described <i>Arabidopsis–Phytophthora</i> pathosystem shows the characteristics of a facultative biotrophic interaction similar to that seen in agronomically important diseases caused by <i>Phytophthora</i> species. In susceptible accessions, extensive colonization of the host tissue occurred and sexual and asexual spores were formed. In incompatible combinations, the plants reacted with a hypersensitive response (HR) and the formation of papillae at the sites of attempted penetration. Defence pathway mutants such as <i>jar1</i> (jasmonic acid-insensitive), <i>etr1</i> (ethylene receptor mutant) and <i>ein2</i> (ethylene-insensitive) remained resistant towards <i>P. porri</i>. However, <i>pad2</i>, a mutant with reduced production of the phytoalexin camalexin, was hyper-susceptible. The accumulation of salicylic acid (SA) and PR1 protein was strongly reduced in <i>pad2</i>. Surprisingly, this lack of SA accumulation does not appear to be the cause of the hyper-susceptibility because interference with SA signalling in <i>nahG</i> plants or <i>sid2</i> or <i>npr1</i> mutants had only a minor effect on resistance. In addition, the functional SA analogue benzothiadiazol (BTH) did not induce resistance in susceptible plants including <i>pad2</i>. Similarly, the complete blockage of camalexin biosynthesis in <i>pad3</i> did not cause susceptibility. Resistance of <i>Arabidopsis</i> against <i>P. porri</i> appears to depend on unknown defence mechanisms that are under the control of PAD2.