Genome-wide identification of NBS-encoding resistance genes in sunflower (Helianthus annuus L.)

Abstract

Nucleotide Binding Site—Leucine-Rich Repeat (NBS-LRR) genes encode disease resistance proteins involved in plants’ defense against their pathogens. Although sunflower is affected by many diseases, only a few molecular details have been uncovered regarding pathogenesis and resistance mechanisms. Recent availability of sunflower whole genome sequences in publicly accessible databases allowed us to accomplish a genome-wide identification of Toll-interleukin-1 receptor-like Nucleotide-binding site Leucine-rich repeat (TNL), Coiled Coil (CC)-NBS-LRR (CNL), Resistance to powdery mildew 8 (RPW8)-NBS-LRR (RNL) and NBS-LRR (NL) protein encoding genes. Hidden Markov Model (HMM) profiling of 52,243 putative protein sequences from sunflower resulted in 352 NBS-encoding genes, among which 100 genes belong to CNL group including 64 genes with RX_CC like domain, 77 to TNL, 13 to RNL, and 162 belong to NL group. We also identified signal peptides and nuclear localization signals present in the identified genes and their homologs. We found that NBS genes were located on all chromosomes and formed 75 gene clusters, one-third of which were located on chromosome 13. Phylogenetic analyses between sunflower and Arabidopsis NBS genes revealed a clade-specific nesting pattern in CNLs, with RNLs nested in the CNL-A clade, and species-specific nesting pattern for TNLs. Surprisingly, we found a moderate bootstrap support (BS = 50%) for CNL-A clade being nested within TNL clade making both the CNL and TNL clades paraphyletic. Arabidopsis and sunflower showed 87 syntenic blocks with 1049 high synteny hits between chromosome 5 of Arabidopsis and chromosome 6 of sunflower. Expression data revealed functional divergence of the NBS genes with basal level tissue-specific expression. This study represents the first genome-wide identification of NBS genes in sunflower paving avenues for functional characterization and potential crop improvement.