The <i>Ptr1</i> Locus of <i>Solanum lycopersicoides</i> Confers Resistance to Race 1 Strains of <i>Pseudomonas syringae</i> pv. <i>tomato</i> and to <i>Ralstonia pseudosolanacearum</i> by Recognizing the Type III Effectors AvrRpt2 and RipBN

Abstract

Race 1 strains of <i>Pseudomonas syringae</i> pv. <i>tomato</i>, which cause bacterial speck disease of tomato, are becoming increasingly common and no simply inherited genetic resistance to such strains is known. We discovered that a locus in <i>Solanum lycopersicoides</i>, termed <i>Pseudomonas tomato race 1</i> (<i>Ptr1</i>), confers resistance to race 1 <i>P. syringae</i> pv. <i>tomato</i> strains by detecting the activity of type III effector AvrRpt2. In <i>Arabidopsis</i>, AvrRpt2 degrades the RIN4 protein, thereby activating <i>RPS2</i>-mediated immunity. Using site-directed mutagenesis of AvrRpt2, we found that, like <i>RPS2</i>, activation of <i>Ptr1</i> requires AvrRpt2 proteolytic activity. <i>Ptr1</i> also detected the activity of AvrRpt2 homologs from diverse bacteria, including one in <i>Ralstonia pseudosolanacearum</i>. The genome sequence of <i>S. lycopersicoides</i> revealed no <i>RPS2</i> homolog in the <i>Ptr1</i> region. <i>Ptr1</i> could play an important role in controlling bacterial speck disease and its future cloning may shed light on an example of convergent evolution for recognition of a widespread type III effector.