Dominant resistance against plant viruses

Abstract

To establish a successful infection plant viruses have to overcome a defense system composed of several layers. This review will overview the various strategies plants employ to combat viral infections with main emphasis on the current status of single dominant resistance (R) genes identified against plant viruses and the corresponding avirulence (Avr) genes identified so far. The most common models to explain the mode of action of dominant R genes will be presented. Finally, in brief the hypersensitive response (HR) and extreme resistance (ER), and the functional and structural similarity of R genes to sensors of innate immunity in mammalian cell systems will be described.

Keywords: ETI; PAMP-triggered immunity; PTI; R genes; RNAi; avirulence; hypersensitive response.

Figure 1

Zig-zag-model. A visual presentation of the arms race between pathogen and host according to Jones and Dangl (2006). Here, a slightly modified version of that model is presented and as described in this review. MAMPs/PAMPs, Microbe/Pathogen associated molecular patterns; PTI, PAMP triggered immunity; ETS, Effector triggered susceptibility; ETI, Effector-triggered immunity; RB, resistance breaker.

Figure 2

Comparison between the structure of plant and animal NLRs. (A) The structure of “Nucleotide binding and leucine rich repeat proteins” (NLRs) from the animal and plant kingdom share highest homology, as all proteins belonging to this class have a C-terminal leucine rich repeat (LRR), a central nucleotide binding domain and a varying N-terminal domain (modified from Maekawa et al., 2011b). Animal TLRs also contain an (extracellular) LRR domain and possess a TIR-domain, they do however, lack a nucleotide binding domain. CC, Coiled-coil; TIR, Toll-interleukin receptor; CARD, Caspase-activation and recruitment domain; PYR, Pyrin domain; BIR, Baculovirus inhibitor-of-apoptosis repeats; NB-ARC, Nucleotide binding and Apaf1-R protein-CED4 domain; NACHT, NAIP – CIITA - HET-E - TP1 domain. (B) A model of NB-LRR R protein recognizing a specific Avr protein through a guardee or decoy host protein. Upon interaction with the Avr protein the R protein conformationally changes and the ADP can be exchanged for ATP, leading to a second conformational change triggering downstream resistance (Modified from Lukasik and Takken, 2009). Whether the R protein returns to its resting state is not known yet. G/D, Guardee/Decoy.