THE OOMYCETE EFFECTOR HARXL106 INDUCES THE SHADE AVOIDANCE SYNDROME IN ARABIDOPSIS BY AFFECTING ITS TRANSCRIPTIONAL REGULATION

BOGINO, MARÍA FLORENCIA; LAPEGNA SENZ, JUAN MARCOS; KOURDOVA, LUCILLE TIHOMIROVA; TAMAGNONE, NICOLÁS; ROMANOWSKI, ANDRES; WIRTHMUELLER, LENNART; FABRO, GEORGINA

Córdoba

Congreso; LX Congreso SAIB 2024; 2024

Sociedad Argentina de Bioquímica y Biología Molecular

Hyaloperonospora arabidopsidis (Hpa) is the obligate oomycete pathogen responsible for causing downy mildew disease in Arabidopsis thaliana. This pathogen secretes numerous effectors proteins which challenge metabolic and signaling processes disrupting plant homeostasis and promoting infection. Our research focuses on the alterations on Arabidopsis’ growth and immunity triggered in response to the effector HaRxL106 from Hpa. Several plant growth regulators are targeted by this effector, including the auxin repressor protein Aux/IAA11, the transcription factor BIM1 that responds to Brassinosteroids and the transcriptional controller RCD1. We found that even grown under normal light conditions, plants constitutively expressing HaRxL106 display a Shade Avoidance-like Syndrome (SAS-like) and are more susceptible to (hemi)biotroph pathogens; these phenotypes are dependent on BIM1 and RCD1, but not on IAA11. Here, we demonstrate how the transcriptional control of a subset of BR and Aux-related genes, which are involved in of the deployment of SAS, is affected by either Hpa infection or HaRxL106 expression in planta. According to transactivation experiments conducted in N. benthamiana, HaRxL106 influences the response of PRE5 and SAUR-AC, two BIM1 target gene promoters. Besides, a substantial quantity of co-expressed genes is observed in the transcriptomes of Col-0 wild type plants treated with far red light at the end of the day (EODFR) and HaRxL106 over-expressor lines (HaRxL106-OE). We additionally examined the degree of responsiveness to EODFR of bim1 and iaa11 mutant lines and HaRxL106-OEs to gain a deeper comprehension of this interplay. Our findings are consistent with the hypothesis that the effector protein HaRxL106 manipulates BIM1 as a host susceptibility factor, which in turn affects the signaling pathways that regulate SAS having a detrimental effect on plant defense responses.