Abstract
Nonexpressor of pathogenesis-related genes 1 (NPR1) is a master regulator of salicylic acid (SA)- facilitated plant hormone signaling and plays a crucial role in plant defense through the activation of systemic acquired resistance (SAR). Although NPR1-like genes are associated with stress responses in a variety of plant species, no thorough genome-wide investigation of these genes has been undertaken in pearl millet (Pennisetum glaucum). This study discovered seven PgNPR1-like genes on four pearl millet chromosomes (Chr1, Chr2, Chr4, and Chr6), which exhibit close affinity to NPRs from other plants and have common gene structures, conserved motifs, and domains. The promoter regions of PgNPR1-like genes have numerous cis-acting elements connected with biotic and abiotic stresses, natural plant growth, and development. The qPCR results showed that PgNPR1-like genes were differentially expressed in distinct tissues, developmental stages, and under various biotic and abiotic stresses. Some putative NPR1-like genes, such as Pgl_GLEAN_10029279, Pgl_GLEAN_10004488, Pgl_GLEAN_10004489, and Pgl_GLEAN_10015079, showed considerable expression in response to abiotic stimuli such as heat, drought, and salinity. The PgNPR1-like gene Pgl_GLEAN_10029279 was observed to be differently expressed upon treatment of hormones such as SA and MeJA. Pgl_GLEAN_10029279 was also significantly expressed after Magnaporthe grisea infection, which causes blast in pearl millet. In silico expression study of the PgNPR1-like genes after Sclerospora graminicola infection, causing downy-mildew disease, revealed that Pgl_GLEAN_10029279 and Pgl_GLEAN_10004489 were significantly upregulated. In addition, the docking results also showed that Pgl_GLEAN_10029279 and Pgl_GLEAN_10007810 out of all seven PgNPRs have strong interactions with the ligand SA, which proves their potential involvement in SA signaling and hence plant defense. These results offer a firm framework for comprehending the roles and development of PgNPR1-like genes in pearl millet.