XopAE effector from Xanthomonas phaseoli pv. manihotis targets HSP20-like p23 cochaperone to suppress plant basal immunity

Gomez De la Cruz, D., Castillo, D. A., Trujillo B., C. A., Medina, C. A., Hurtado, V., Gil, J., Padmanabhan, M., Restrepo, S., Dinesh-Kumar, S. P., Germain, H., Lopez, C. et Bernal, A. (2025). XopAE effector from Xanthomonas phaseoli pv. manihotis targets HSP20-like p23 cochaperone to suppress plant basal immunity. Molecular Plant-Microbe Interactions®, 38 (3). pp. 365-375. ISSN 0894-0282 1943-7706 DOI 10.1094/MPMI-08-24-0086-R

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Résumé

Abstract

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 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 (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, while 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 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.

Type de document:	Article
Date de dépôt:	25 mars 2025 17:47
Dernière modification:	28 juill. 2025 14:04
Version du document déposé:	Version officielle de l'éditeur
URI:	https://depot-e.uqtr.ca/id/eprint/11773

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