The basidiomycete Piriformospora indica colonizes roots of a multitude of plants therebytransferring several beneficial effects such as growth promotion as well as enhanced local andsystemic resistance against pathogens (Varma et al., 1999; Waller et al., 2005; Deshmukh andKogel, 2007; Stein et al., 2008). The wide host range of P. indica implicates that the fungushas developed effective strategies to overcome plant innate immunity. Recent cytologicalstudies on P. indica-colonized Arabidopsis roots revealed that the fungus has developed aninitial biotrophic colonization strategy followed by a cell death-associated colonizationpattern (Jacobs, Zechman, Kogel, Schäfer, unpublished). It was the aim of my project toanalyze the genetic, molecular, and biochemical mechanisms of P. indica-mediated cell deathduring root colonization. Cell biological analyses uncovered an impaired ER integrity as wellas vacuolar collapse at later cell-death-associated fungal colonization stages. Subsequentpharmacological analyses confirmed ER stress induction by P. indica, but molecular andbiochemical analyses suggested suppression of ER stress signaling, known as unfoldedprotein response, by the fungus. Based on biochemical and genetic experiments, I provideevidence that colonization-associated cell death is initiated by an uncoupled ER stresssignaling. My data raises the possibility that the emerging ER stress activates a cell deathprogramme, whose execution is dependent on the caspase-1 activity mediated byvacuole-localized vacuolar processing enzymes (VPEs). I propose a model in which P. indicais impairing ER integrity to induce VPE/caspase 1-dependent cell death. In addition, thefungus might interfere with ER functionality to disturb root MAMP-triggered immunity. Thecombined inhibitory activity might ultimately enhance the fungus´ ability to colonize roots.
