Breaking or sneaking into the fortress: the root endodermis is a defence wall against nematode infection

Roots are a truly amazing plant structure: they conquer the underground, form complex structures that anchor the plant, let water and nutrients in, but must not dry out. Roots store energy, send signals to the aboveground parts of the plant and to neighbors, and defend the plant against soil-borne pathogens. Within the root, the endodermis is the barrier that separates the inner vasculature from the outer cortex. If the root is a fortress, the endodermis is the gated wall. Cell wall reinforcements such as the casparian strip (CS), lignin deposition, and suberin seal the apoplast of the endodermis throughout different parts of the root. These reinforcements allow the diffusion of water and nutrients to and from the vascular tissue while blocking its penetration by pathogens such as bacteria and fungi (Enstone et al., 2002). But roots also face pathogens of a different kind: root-infecting, sedentary endoparasites such as cyst nematodes (CNs) and root-knot nematodes (RKNs). These pathogens infect a variety of important crops and cause significant yield losses (Savary et al., 2019). Does the endodermis also help protect plants from nematodes? Holbein et al. (2019) set out to answer this question in the current issue of The Plant Journal. Cyst nematodes such as Heterodera spp. and Globodera spp. can break ‘through the walls’, i.e., cross the endodermis directly and penetrate vascular tissues at any root zone. Inside the root, CNs move intercellularly to reach the vascular cylinder, where they establish a feeding site. In contrast, RKNs such as Meloidogyne spp. enter through ‘gaps in the wall’: they penetrate the root at the elongation zone of the root tip, where there are no endodermal barriers. Then, they move within the cortex to the root meristem, where they enter the vascular cylinder (Holbein et al., 2016). The study looked at the role of suberin and the CS in plant-nematode interactions using Arabidopsis as a model, the beet CN Heterodera schachtii, and the RKN Meloidogyne incognita. Using fluorescent microscopy, a variety of promoter::reporter lines, and well-established markers for different tissues, they demonstrate that the endodermis surrounds infection sites during the early stages of both CN and RKN infections. However, the endodermis degrades a few days later, and suberization or periderm formation follows. The results suggest that nematode infection causes damage to the endodermis and induces periderm development, which is coordinated with the upregulation of suberin biosynthesis genes at the site of infection. The authors then used mutants defective in suberin deposition, CS formation, or both to characterize the role of the endodermis during plant-nematode interactions. The results show that the double mutants are significantly more susceptible to nematode parasitism (see Figure).