Plant basal resistance to nematodes: an update

Abstract

Most plant-parasitic nematodes are obligate biotrophs feeding on the roots of their hosts. Whereas ectoparasites remain on the root surface and feed on the outer cell layers, endoparasitic nematodes enter the host to parasitize cells around or within the central cylinder. Nematode invasion and feeding causes tissue damage which may, in turn, lead to the activation of host basal defence responses. Hitherto, research interests in plant-nematode interaction have emphasized effector-triggered immunity rather than basal plant defence responses. However, some recent investigations suggest that basal defence pathways are not only activated but also play an important role in determining interaction outcomes. In this review we discuss the major findings and point out future directions to dissect the molecular mechanisms underlying plant basal defence to nematodes further.

Plant-parasitic nematodes: towards understanding molecular players in stress responses

“…However, DAMPs have not yet been identified in plant–nematode interactions. Although the activation of basal defence responses remains underexplored, numerous reviews have shed light on their relevance to identify key molecular players that are involved at early stages of infection (Feng and Shan, 2014; Holbein et al , 2016). …”

“…It seems that PAO enzymatic activity plays a pivotal role in cellular redox homeostasis in response to pathogen infection. Following these findings, it was proposed that PPNs might modulate the production of reactive species, not as toxic compounds, but as signalling molecules to activate antioxidant pathways (Goverse and Smant, 2014; Holbein et al , 2016). …”

“…As summarized in the classic zig-zag model, defence is based on (1) perception of conserved microbial-associated molecular patterns (MAMPs) or pathogen-associated molecular patterns (PAMPs) by cell surface-localized pattern recognition receptors (PRRs) that initiates basal immunity known as MTI/PTI (MAMP- or PAMP-triggered immunity) and (2) recognition of pathogenic effectors by intracellular nucleotide-binding domain leucine-rich repeat proteins (NB-LRRs) leading to effector-triggered immunity (ETI) (Jones and Dangl, 2006; Dodds and Rathjen, 2010). Although our knowledge of immune signalling components is currently poor with regard to plant/nematode interactions, molecular mechanisms of plant defence imply a certain degree of conservation among a broad range of studied pathosystems (Goverse and Smant, 2014; Zipfel, 2014; Holbein et al , 2016). During the early stages of infection, plant recognition of plant-parasitic nematodes (PPNs) leads rapidly to the production of reactive species [reactive oxygen (ROS) and reactive nitrogen (RNS)] and toxic molecules derived from secondary metabolism (Melillo et al , 2011).…”

Arabidopsis leucine-rich repeat receptor–like kinase NILR1 is required for induction of innate immunity to parasitic nematodes

“…To date, no PRR that recognises a nematode-associated molecular pattern (NAMP) has been identified [18]. However, some recent work suggests that nematode infection triggers PTI responses in host through surface-localised receptors.…”

Elevated CO2 and warming shift the functional composition of soil nematode communities in a semiarid grassland

“…Finally, Suseela et al (in review) observed positive, and sometimes sub-additive, effects of eCO 2 and warming on the amount of suberin and individual suberin monomers in plant roots. If these plant biomolecules inhibit plantfeeding nematodes (Biederman and Boutton, 2009;Holbein et al, 2016), this result could help explain the negative, sub-additive effects of eCO 2 and warming on the abundance of plant-feeding nematodes (Fig. 1).…”