Plant growth-regulating hormonal pathways are targeted by two effectors belonging to evolutionary unrelated filamentous pathogens.

LAPEGNA SENZ, JUAN MARCOS; BOGINO, MARÍA FLORENCIA; FABRO, GEORGINA

Rosario

Congreso; XXXIV Reunión Argentina de Fisiología Vegetal; 2023

Sociedad Argentina de Fisiología Vegetal

Plant pathogens evolved several ways to colonize their hosts. Proteinaceous effectors are part of the weaponry they deploy to subvert plant defenses. Filamentous pathogens release effectors into the apoplast or the cytoplasm of plant cells, where they interfere with multiple host’s metabolisms.Interactomics’ experiments reported that effector OEC115 from the fungus Golovinomyces orontii interacts with two Arabidopsis’ proteins, BIM1 and IAA11, which participate from the Brassinosteroids and Auxins signaling pathways, respectively. Many reports describe the involvement of these hormones in defense responses; however, the specific functions of BIM1 and IAA11 in plant immunity remain unclear. Interestingly, we previously found another effector, HaRxL106 from the oomycete pathogen Hyaloperonospora arabidopsidis, that also interacts with BIM1 and IAA11. Here we confirmed the interaction of OEC115 with BIM1 and IAA11 by Yeast-two-Hybrid (Y2H) and Bimolecular Fluorescence Complementation (BiFC) assays. Both effectors, as well as their targets, localize in the nucleus of plant cells. Surprisingly, OEC115 and HaRxL106 have no similarities in their aminoacidic sequence, suggesting that their activities over BIM1 and IAA11 could be different. Indeed, when we developed infection assays on 35S:GFP-OEC115 overexpressing plants with Pseudomonas syringae pv. tomato, we observed that, unlike HaRxL106 overexpressors, these plants were not more susceptible than the wild type. Moreover, 35S:GFP-OEC115 plants do not present visible abnormal developmental phenotypes, as plants expressing HaRxL106 do. The evolutionary convergence of these effectors towards the same host proteins is intriguing, given that these two non-related pathogens manipulate the same “targets” but with different phenotypic outputs. We present our perspectives to further investigate these effectors’ molecular mechanisms to tamper plant defenses and/or growth.