SNPs, InDels, and Microsatellites within and Near to Rice NBS-LRR Resistance Gene Candidates

Mark J Quinton-Tulloch,Katherine A Steele

doi:10.3390/agronomy11112297

Abstract

Plant resistance genes (R-genes) drive the immune responses of crops against specific pathotypes of disease-causing organisms. Over time, genetic diversity in R-genes and R-pseudogenes has arisen among different rice varieties. This bioinformatics study was carried out to (i) predict the full sets of candidate nucleotide-binding site leucine-rich repeat (NLR) R-genes present in six rice genomes; (ii) detect variation within candidate R-genes; (iii) identify potential selectable markers within and near to LRR genes among 75 diverse indica rice genomes. Four high quality indica genomes, plus the standard japonica and indica reference genomes, were analysed with widely available bioinformatic tools to identify candidate R-genes and R-pseudogenes. They were detected in clusters, consistent with previous studies. BLAST analysis of cloned protein sequences of 31 R-gene loci gave confidence in this approach for detection of cloned NLR R-genes. Approximately 10% of candidate R-genes were located within 1 kb of a microsatellite (SSR) marker. Sequence comparisons among indica rice genomes detected SNPs or InDels in 334 candidate rice R-genes. There were significantly more SNPs and InDels within the identified NLR R-gene candidates than in other types of gene. The genome-wide locations of candidate R-genes and their associated markers are presented here for the potential future development of improved disease-resistant varieties. Limitations of in silico approaches used for R-gene discovery are discussed.

Highlights

Plant pathogens contribute to yield losses of up to 30% of global rice (Oryza sativaL.) production, leading to as much as 40.9% of crop losses in some major food security hotspots [1]
Some effector-triggered immunity (ETI) and pathogen-associated molecular patterns (PAMPs)-triggered immunity (PTI) genes can contribute to quantitative disease resistance, several other mechanisms can be involved in quantitative resistance [2]
There was a significant amount of overlap between the sets of genes identified, many were not identified as resistance genes (R-genes) in some genomes by either of the motif-searching methods

Summary

Introduction

Plant pathogens contribute to yield losses of up to 30% of global rice (Oryza sativaL.) production, leading to as much as 40.9% of crop losses in some major food security hotspots [1]. PAMP-triggered immunity (PTI) involves the recognition of conserved pathogen-associated molecular patterns (PAMPs), essential for pathogen survival, by host cell surface transmembrane pattern recognition receptors (PRRs). This triggers intracellular signalling events and changes in host gene expression that restrict microbial movement within the host. Nonhost-specific resistance is generally considered to be controlled by PTI. ETI controls host-specific resistance through recognition of pathogen effectors, known as avirulence genes, that encode species-, race-, or even strain-specific proteins. Plants have coevolved specific resistance (R) genes, which encode cytoplasmic protein receptors that bind to the complementary avirulence proteins and activate ETI, often leading to localised cell death that prevents pathogen spread [2]. Some ETI and PTI genes can contribute to quantitative disease resistance, several other mechanisms can be involved in quantitative resistance [2]

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