The Lectin Receptor Kinase LecRK-I.9 Is a Novel Phytophthora Resistance Component and a Potential Host Target for a RXLR Effector

Abstract

In plants, an active defense against biotrophic pathogens is dependent on a functional continuum between the cell wall (CW) and the plasma membrane (PM). It is thus anticipated that proteins maintaining this continuum also function in defense. The legume-like lectin receptor kinase LecRK-I.9 is a putative mediator of CW-PM adhesions in Arabidopsis and is known to bind in vitro to the Phytophthora infestans RXLR-dEER effector IPI-O via a RGD cell attachment motif present in IPI-O. Here we show that LecRK-I.9 is associated with the plasma membrane, and that two T-DNA insertions lines deficient in LecRK-I.9 (lecrk-I.9) have a ‘gain-of-susceptibility’ phenotype specifically towards the oomycete Phytophthora brassicae. Accordingly, overexpression of LecRK-I.9 leads to enhanced resistance to P. brassicae. A similar ‘gain-of-susceptibility’ phenotype was observed in transgenic Arabidopsis lines expressing ipiO (35S-ipiO1). This phenocopy behavior was also observed with respect to other defense-related functions; lecrk-I.9 and 35S-ipiO1 were both disturbed in pathogen- and MAMP-triggered callose deposition. By site-directed mutagenesis, we demonstrated that the RGD cell attachment motif in IPI-O is not only essential for disrupting the CW-PM adhesions, but also for disease suppression. These results suggest that destabilizing the CW-PM continuum is one of the tactics used by Phytophthora to promote infection. As countermeasure the host may want to strengthen CW-PM adhesions and the novel Phytophthora resistance component LecRK-I.9 seems to function in this process.

Nicotiana attenuata LECTIN RECEPTOR KINASE1 Suppresses the Insect-Mediated Inhibition of Induced Defense Responses during Manduca sexta Herbivory

“…For example, the rice Pi-d2 LecRK protein participates in the resistance mechanisms against Magnaporthe grisea (Chen et al, 2006) and RLK1 from N. glutinosa participates in the resistance mechanisms against Phytophthora capsici (Kim et al, 2010). In the group of L-type LecRKs, LRK1 from N. benthamiana interacts with the Phytophthora infestans elicitin INF1 and triggers INF1-induced cell death (Kanzaki et al, 2008), and the Arabidopsis thaliana LecRK-I.9 has been identified as a putative mediator of cell wall-plasma membrane adhesion during infection with Phytophthora species (Bouwmeester et al, 2011). LecRK-I.9 binds to a P. infestans effector protein through an RGD (Arg-Gly-Asp) motif that is also present as a cell attachment motif in extracellular matrix proteins that mediate cell adhesion to the cell walls (Bouwmeester et al, 2011).…”

The Lectin Receptor Kinase-VI.2 Is Required for Priming and Positively Regulates Arabidopsis Pattern-Triggered Immunity

“…In Nicotiana attenuata, LecRK1 was shown to suppress insect-mediated inhibition of jasmonic acid-induced defense responses (Gilardoni et al, 2011). Another LecRK with a potential role in plant defense is the Arabidopsis LecRK79/LecRK-I.9 (Gouget et al, 2006;Bouwmeester et al, 2011).…”

Mechanisms of Nuclear Suppression of Host Immunity by Effectors from the Arabidopsis Downy Mildew Pathogen Hyaloperonospora arabidopsidis (Hpa)

“…For this reason, we analyzed stable effector expression in planta, particularly for studying Arabidopsis-compatible pathosystems. Stable effector expression in planta allows us to test whether the ectopic expression of a given effector affects plant susceptibility toward the corresponding pathogen (Bozkurt et al 2011;Fabro et al 2011;Caillaud et al 2012) or even other pathogens (van Esse et al 2008;Hewezi et al 2010;Bouwmeester et al 2011;Fabro et al 2011). Using this approach, effectors from Hpa, including ATR13, were shown to suppress plant defenses, notably PAMP-induced ROS burst and callose deposition, which are typical indicators of plant immune response activation (Sohn et al 2007;Fabro et al 2011).…”