The XopAE Effector from Xanthomonas phaseoli pv. manihotis Targets HSP20-like p23 Cochaperone to Suppress Plant Basal Immunity

Pathogenic bacteria use Type 3 effector proteins to manipulate host defenses and alter metabolism to favor their survival and spread. The non-model bacterial pathogen Xanthomonas phaseoli pv. manihotis (Xpm) causes devastating disease in cassava. The molecular role of Type 3 effector proteins from Xpm in causing disease is largely unknown. Here, we report that the XopAE effector from Xpm suppresses plant defense responses. Our results show that XopAE is a suppressor of basal defenses such as callose deposition and the production of reactive oxygen species. XopAE targets a small heat shock protein (Mep23-1 cochaperone) in cassava and its homolog Atp23-1 in Arabidopsis. XopAE localizes to the nucleus and in scattered points throughout the cell border, whereas Mep23-1 shows a nucleocytoplasmic localization. Upon interaction, XopAE hijacks Mep23-1 to the scattered points throughout the cell border, and they also interact in the nucleus. Our results indicate that the interaction between XopAE and Mep23-1 is essential for suppressing basal plant defense. This study is one of the first to address the molecular mechanisms deployed by Xpm to cause disease in cassava, a non-model crop plant.