Abstract
The majority of disease resistance (R) genes identified to date in plants encode a nucleotide-binding site (NBS) and leucine-rich repeat (LRR) domain containing protein. Additional domains such as coiled-coil (CC) and TOLL/interleukin-1 receptor (TIR) domains can also be present. In the recently sequenced Solanum tuberosum group phureja genome we used HMM models and manual curation to annotate 435 NBS-encoding R gene homologs and 142 NBS-derived genes that lack the NBS domain. Highly similar homologs for most previously documented Solanaceae R genes were identified. A surprising ∼41% (179) of the 435 NBS-encoding genes are pseudogenes primarily caused by premature stop codons or frameshift mutations. Alignment of 81.80% of the 577 homologs to S. tuberosum group phureja pseudomolecules revealed non-random distribution of the R-genes; 362 of 470 genes were found in high density clusters on 11 chromosomes.
Highlights
Plants have developed different strategies to protect themselves from pathogens
Numerous R genes have been cloned from a wide range of angiosperms [1,2].The most predominant disease resistance genes cloned to date, the nucleotide-binding site (NBS)-leucinerich repeat (LRR) resistance genes, encode proteins containing nucleotide binding (NBS) sites and leucine-rich (LRR) repeat domains
It is well known that the NBS domain of resistance genes has some conserved motifs that allow distinguishing between CNL and TNL proteins
Summary
Plants have developed different strategies to protect themselves from pathogens. Innate resistance in plants can trigger a powerful set of inducible defense responses. One of the most studied mechanisms of defense is mediated by the disease resistance proteins that function in the recognition of pathogen effectors. Numerous R genes have been cloned from a wide range of angiosperms [1,2].The most predominant disease resistance genes cloned to date, the NBS-LRR resistance genes, encode proteins containing nucleotide binding (NBS) sites and leucine-rich (LRR) repeat domains. They can, contain additional domains in their amino- and carboxy-terminal domains [3]. Activation of R genes results in cell death through the onset of the hypersensitive response (HR) [6,7,8]
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