An Oomycete effector alters plant immunity and development by manipulating auxin signaling.

BOGINO, MARÍA FLORENCIA; WIRTHMUELLER, LENNART; FABRO, GEORGINA

Mendoza

Congreso; Congreso de la Sociedad Argentina de Investigaciones en Bioquímica y Biología Molecular 2022; 2022

Sociedad Argentina de Investigaciones en Bioquímica y Biología Molecular

The biotrophic oomycete Hyaloperonospora arabidopsidis has co-evolved with its only host, Arabidopsis thaliana. The study of their compatible/incompatible interactions has contributed to the construction of the “arms race” hypothesis. According to this, pathogens developed virulent effectors that can suppress the first layer of plant immune responses, known as PAMP-triggered immunity. Meanwhile, plants co-evolved resistance genes that trigger Effector-triggered immunity (ETI), but some effectors are able to suppress ETI and so on. Among the plant targets of pathogen’s effectors, are host proteins involved in growth and development. It has been proposed that certain pathogens can manipulate the growth-defense trade-off on their own benefit, tampering hormonal pathways to suppress plant immunity and maintain compatibility with the host. We have previously observed an activation of the Auxin responsive DR5:GUS reporter in Hpa infected plants, suggesting that the auxin signaling pathway was induced during a compatible interaction. Thus, we set up to investigate the role of an Hpa effector that, when was expressed in an estradiol-inducible manner in the DR5:GUS reporter background, partially recapitulated the phenotype observed with the whole pathogen. Here we describe our findings regarding the effector HaRxL106: 1) It interacts with a component of the Arabidopsis auxin-signaling pathway (IAA11) as we could confirm via BiFC and Yeast-Two-Hybrid assays. 2) The interaction of IAA11 is stronger with the C-terminal part, than with the N-terminal of HaRxL106. 3) The overexpression of the effector in wild type as well as iaa11 mutant plants generated an altered growth phenotype with elongated hypocotyls and petioles and a curved narrow leaf lamina, reminiscent of the shade-avoidance syndrome displayed by plants experiencing persistent shadow. 4) iaa11 mutant plants are more susceptible to Hpa and to the bacteria Pseudomonas syringae DC3000 than wild type plants. 5) Upon Hpa infection some Auxin responsive genes are induced. Based on the above-mentioned results, we propose a working model where HaRxL106 negatively influences the repressor activity of IAA11, probably releasing one or more ARF transcription factors, that would then induce the transcription of Auxin responsive genes. The activation of Auxin signaling, due to the trade-off between growth and defense, could contribute to the enhancement of the plant susceptibility to Hpa.