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

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.