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. 2015 Mar 5:6:134.
doi: 10.3389/fpls.2015.00134. eCollection 2015.

The "sensor domains" of plant NLR proteins: more than decoys?

Chih-Hang Wu  1 , Ksenia V Krasileva  2 , Mark J Banfield  3 , Ryohei Terauchi  4 , Sophien Kamoun  1
Affiliations

The "sensor domains" of plant NLR proteins: more than decoys?

Chih-Hang Wu et al. Front Plant Sci. .
No abstract available

Keywords: Arabidopsis thaliana; NLR protein pairs; decoy; integrated decoy; pathogen recognition; plant immunity; rice; sensor domain.

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Figures

Figure 1
Figure 1
A genetic test to inform whether NLR-SD proteins have retained a biochemical activity independent of perception of an avirulence effector. In the top panel, isogenic plants either carrying or lacking the NLR-SD display differential resistance to a pathogen strain carrying the AVR (avirulence) effector (top panel, NLR-SD plants displaying full resistance to the avirulent pathogen strain). To challenge the decoy hypothesis, the differential NLR-SD lines are challenged with a pathogen strain that lacks the AVR effector (avr) and is isogenic to the AVR strain. In these experiments, three outcomes can be expected. (1) No differences between the NLR-SD lines are observed resulting in inconclusive results—the null decoy hypothesis cannot be rejected. The reason the result is inconclusive is because it is now accepted that effectors have other activities than suppression of immunity (nutrition, development, epigenetics etc.), and therefore the targeted host proteins do not necessarily modulate susceptibility/resistance phenotypes. (2) The plants carrying the NLR-SD are more resistant to the avr pathogen strain that lacks the AVR effector. (3) The plants carrying the NLR-SD are more susceptible to the avr pathogen strain that lacks the AVR effector. In these two cases, the SD is likely to have retained the biochemical activity of its ancestral host protein and the decoy hypothesis can be rejected. In scenario (2), the higher levels of resistance to the avr pathogen conferred by the NLR-SD are consistent with a role of the SD in basal immunity analogous to the ancestral target. In scenario (3), however, the NLR-SD is more susceptible to its isogenic line possibly because the SD is targeted by another (unrecognized) effector. In such a case, the NLR-SD resistance (R) gene becomes a susceptibility (S) gene depending on the genotype of the pathogen it is challenged with.
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