Paleo-evolutionary plasticity of plant disease resistance genes

Rongzhi Zhang,Florent Murat,Thierry Langin,Jerome Salse,Caroline Pont

doi:10.1186/1471-2164-15-187

Abstract

BackgroundThe recent access to a large set of genome sequences, combined with a robust evolutionary scenario of modern monocot (i.e. grasses) and eudicot (i.e. rosids) species from their founder ancestors, offered the opportunity to gain insights into disease resistance genes (R-genes) evolutionary plasticity.ResultsWe unravel in the current article (i) a R-genes repertoire consisting in 7883 for monocots and 15758 for eudicots, (ii) a contrasted R-genes conservation with 23.8% for monocots and 6.6% for dicots, (iii) a minimal ancestral founder pool of 384 R-genes for the monocots and 150 R-genes for the eudicots, (iv) a general pattern of organization in clusters accounting for more than 60% of mapped R-genes, (v) a biased deletion of ancestral duplicated R-genes between paralogous blocks possibly compensated by clusterization, (vi) a bias in R-genes clusterization where Leucine-Rich Repeats act as a ‘glue’ for domain association, (vii) a R-genes/miRNAs interome enriched toward duplicated R-genes.ConclusionsTogether, our data may suggest that R-genes family plasticity operated during plant evolution (i) at the structural level through massive duplicates loss counterbalanced by massive clusterization following polyploidization; as well as at (ii) the regulation level through microRNA/R-gene interactions acting as a possible source of functional diploidization of structurally retained R-genes duplicates. Such evolutionary shuffling events leaded to CNVs (i.e. Copy Number Variation) and PAVs (i.e. Presence Absence Variation) between related species operating in the decay of R-genes colinearity between plant species.

Highlights

IntroductionThe recent access to a large set of genome sequences, combined with a robust evolutionary scenario of modern monocot (i.e. grasses) and eudicot (i.e. rosids) species from their founder ancestors, offered the opportunity to gain insights into disease resistance genes (R-genes) evolutionary plasticity
The recent access to a large set of genome sequences, combined with a robust evolutionary scenario of modern monocot and eudicot species from their founder ancestors, offered the opportunity to gain insights into disease resistance genes (R-genes) evolutionary plasticity
Conservation and evolutionary patterns To identify the largest set of plant R-genes, three complementary methods were combined consisting in (1) the detection of PFAM [64] domains, (2) the exploitation of public genome annotations, and (3) the use of the Plant Resistance Gene Database, PRGdb

Summary

Introduction

The recent access to a large set of genome sequences, combined with a robust evolutionary scenario of modern monocot (i.e. grasses) and eudicot (i.e. rosids) species from their founder ancestors, offered the opportunity to gain insights into disease resistance genes (R-genes) evolutionary plasticity. Plants have developed a battery of defense mechanisms involving (1) PTI (PAMP-Triggered Immunity) triggered by PAMP (Pathogen-Associated Molecular Patterns) [5,6,7] and (2) ETI (Effector-Triggered Immunity) triggered by effectors leading to hypersensitive response (referenced as HR [8]). Repeats (LRR) [9,10], Toll-Interleukine Receptors (TIR), WRKY transcription factors [11,12], Lysine Motif (LysM) families [13,14], and Protein Kinase families (hereafter referenced as PKinase) [15,16]. WRKY and protein-kinases, associated with protein domains encoded by R-genes (hereafter R-domains), can be activated by PRRs in disease resistance pathways [18,19,20]

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Conclusion