An oomycete effector alters plant immunity and development by manipulating auxin signaling

BOGINO MARIA FLORENCIA; LENNART WIRTHMUELLER; FABRO GEORGINA

Mendoza

Congreso; LVIII Reunión Anual SAIB; 2022

Sociedad Argentina de Bioquímica y Biología Molecular

The biotrophic oomycete Hyaloperonospora arabidopsidis has co-evolved with its host, Arabidopsis thaliana. The study of their interaction contributed to postulate the “arms race” hypothesis between plants and pathogens. According to it, pathogens evolutionarily develop effectors that can suppress the first layer of plant immune responses induced by their conserved molecules or PAMPs, which is known as PAMP-Triggered Immunity (PTI). Similarly, plants co-evolved resistance genes/proteins that recognize these effectors, thus triggering Effector-Triggered Immunity (ETI). Interestingly, some effectors are also able to suppress ETI, but can become recognized by the plant and so on. Plant proteins involved in growth and development are among the host targets of pathogen’s effectors. It has been proposed that certain pathogens can manipulate the growth-defense trade-off on their own benefit, tampering hormonal pathways to suppress PTI and maintain compatibility with the host. We have previously observed an activation of the auxin responsive DR5:GUS reporter gene 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 (HaRxL106) that, when expressed in an estradiol-inducible manner in the DR5:GUS background, partially recapitulated the phenotype observed with the whole pathogen. Here we describe our findings regarding this effector: 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) Upon Hpa compatible interaction, auxin responsive genes are induced; 4) The overexpression of the effector in wild type background, as well as in 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; 5) iaa11 mutant plants are more susceptible to Hpa and to the bacteria Pseudomonas syringae DC3000 than wild type plants. 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 thetranscription of auxin responsive genes. This activation of auxin signaling apparently contributes to the enhancement of the susceptibility to Hpa.