1. A molecular evolutionary concept connecting nonhost resistance, pathogen host range, and pathogen speciation 
Paul Schulze-Lefert, Ralph Panstruga 
Trends in Plant Science 
Volume 16, Issue 3, Pages (March 2011)
DOI: /j.tplants
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2. Figure 1
Relative contribution of NB-LRR- and PRR-triggered immunity to nonhost resistance. The chart illustrates the supposed relative contribution of NB-LRR-triggered (blue) and PRR-triggered (red) immunity to nonhost resistance against a given pathogen as a function of the evolutionary distance of the authentic host plant species of that pathogen to an assumed nonhost species. The model is based on two assumptions: (i) the proportion of pathogen effectors that fail to ‘find’ corresponding targets raises with increasing divergence time between host and non-host, and (ii) the co-evolutionary arms race in host-adapted interactions and concomitant changes in NB-LRR and effector repertoires ‘depletes’ the capacity of phylogenetically distant nonhosts to recognize effectors of host-adapted pathogens.
Trends in Plant Science  , DOI: ( /j.tplants )
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3. Figure 2
Effector and NB-LRR gene evolution during co-speciation and host jumps. The scheme illustrates the evolution of host NB-LRR (colored squares) and pathogen effector gene (colored circles) repertoires following co-speciation or host jumps. In the last common ancestor (A) of two plant species, (B) and (C), few pathogen effectors match cognate NB-LRR proteins (indicated by corresponding colors and connecting arrows with arrowheads on either side), leading to pathogen strain- and host accession-dependent immunity or pathogen colonization. Shortly after speciation of plants (B) and (C) the last common pathogen species is still able to colonize both plant species (indicated by arrows with dashed lines). Following a period of co-evolution of both new host–parasite pairs, new complementary NB-LRR gene-effector gene pairs appear. The emergence of (B) or (C) specific NB-LRR proteins recognizing conserved effectors and/or the deletion of conserved effectors drives the pathogen into reproductive isolation by preventing further cross-infection. Pathogens can also colonize new phylogenetically distant plant habitats (D) by ‘host jumps’ following large-scale effector diversification by one of the five molecular mechanisms outlined in the main text. Upon a period of co-evolution, new complementary NB-LRR gene-effector gene pairs emerge also in this scenario.
Trends in Plant Science  , DOI: ( /j.tplants )
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4. Figure 3
A comparison of host and pathogen phylogenies reveals co-speciation and host jumps. Depicted are the fictitious species phylogenies of a taxonomic group of plant hosts (left; species A–H) and their adapted pathogens (right, species a–h; matching plant parasite pairs are connected by a dashed line). Plant and pathogen phylogenies are largely congruent, indicative of plant–parasite co-speciation (see Figure 2), except for the couple E/e, which is the result of a host jump of pathogen species e.
Trends in Plant Science  , DOI: ( /j.tplants )
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