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 pv. () causes devastating disease in cassava. The molecular role of Type 3 effector proteins from in causing disease is largely unknown. Here, we report that the XopAE effector from suppresses plant defense responses. Our results showed that XopAE is a suppressor of basal defenses such as callose deposition and the production of reactive oxygen species (ROS). XopAE targets a small heat shock protein (p23-1 cochaperone) in cassava and its homolog p23-1 in . XopAE localizes to the nucleus and in scattered points throughout the cell border, while p23-1 shows a nucleocytoplasmic localization. Upon interaction, XopAE hijacks p23-1 to the scattered points throughout the cell border and they also interact in nucleus. Our results indicate that the interaction between XopAE and p23-1 is essential for suppressing basal plant defense. This study is one of the first to address the molecular mechanisms deployed by to cause disease in cassava, a non-model crop plant.
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http://dx.doi.org/10.1094/MPMI-08-24-0086-R | DOI Listing |
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