Molecular mechanisms that limit the costs of NLR-mediated resistance in plants

Abstract

Crop diseases cause significant yield losses, and the use of resistant cultivars can effectively mitigate these losses and control many plant diseases. Most plant resistance (R) genes encode immune receptors composed of nucleotide-binding and leucine-rich repeat (NLR) domains. These proteins mediate the specific recognition of pathogen avirulence effectors to induce defence responses. However, NLR-triggered immunity can be associated with a reduction in growth and yield, so-called 'fitness costs'. Recent data have shown that plants use an elaborate interplay of different mechanisms to control NLR gene transcript levels, as well as NLR protein abundance and activity, to avoid the associated cost of resistance in the absence of a pathogen. In this review, we discuss the different levels of NLR regulation (transcriptional, post-transcriptional and at the protein level). We address the apparent need for plants to maintain diverse modes of regulation. A recent model suggesting an equilibrium 'ON/OFF state' of NLR proteins, in the absence of a pathogen, provides the context for our discussion.

Keywords: cost; methylation; plant disease resistance genes; post-transcriptional regulation; small RNAs; transcriptional regulation.