Molecular Cloning, Bioinformatics, and Expression Analysis of the NPR1 Homolog in Sesame (Sesamum indicum L.)

Sesame bacterial wilt, caused by the pathogen <i>Ralstonia solanacearum</i>, is a major constraint for continuous cropping. Deciphering the defense mechanisms of sesame is therefore essential to the development of novel and effective control strategies. The <i>Non-expressor of Pathogenesis-Related</i> 1 (NPR1) plays a key role in regulating salicylic acid (SA)-mediated systemic acquired resistance (SAR). In this study, we reported that leaf treatments with 50 μg/mL benzothiadiazole (BTH) resulted in increased protection of sesame against <i>Ralstonia solanacearum</i>. We clarified the structure, expression patterns, and function of a <i>NPR1</i> homologous gene, <i>SiNPR1</i>, in sesame. The <i>SiNPR1</i> gene open reading frame comprises 1758 bp, and it encodes 585 amino acids. Phylogenetic analysis revealed that SiNPR1 is closely related to NPR1-like in <i>Olea europaea</i> and clustered with other members of the families Monocotyledon and Dicotyledon. Quantitative real-time PCR (qRT-PCR) results demonstrated that the expression of the <i>SiNPR1</i> gene was organ-specific and could be induced by BTH. The yeast two-hybrid assay confirmed that SiNPR1 directly interacts with SiTGA2. In conclusion, these results suggest that SiNPR1 plays a pivotal role in the BTH-dependent systemic acquired resistance in sesame.