Altered metabolomic profile of selected metabolites and improved resistance of Cicer arietinum (L.) against Meloidogyne incognita (Kofoid & White) Chitwood following seed soaking with salicylic acid, benzothiadiazole or nicotinic acid

The seeds of chickpea Cicer arietinum (L.) were soaked in 0.00, 10.0 or 20.0 mu g/mL of salicylic acid (SA), benzothiadiazole (BTH) or nicotinic acid (NA) solutions for 1 h. Treated seeds were sown in field and metabolite profiling of free reduced/oxidized glutathione (GSH/GSSG), SA, acetyl salicylic acid (ASA), jasmonic acid (JA), and chlorogenic acid (CGA) in chickpea crop was carried out at regular intervals (15, 30, 60, 90 and 120 days of sowing) using liquid chromatography (LC). These defense activators increased the levels of GSH, SA, and CGA in leaf; GSSG, ASA, and JA in root; and decreased the levels of GSSG and JA in leaf; GSH, SA, and CGA in root. In leaf, the biosynthesis of SA increased concomitantly with that of GSH. ASA and JA levels declined with increase of SA concentration. CGA biosynthesis increased with decline of JA level. In root, CGA and SA levels declined with increase of JA concentration. The SA level was directly related to CGA and inversely to ASA and JA concentrations. The CGA and SA concentrations increased with treatment dosage up to 120 days. The concentration of leaf GSSG was linked with JA level in root. Chickpea was a SA-rich crop. GSH in leaf was the key metabolite for SA and JA signaling. The reduction in root infection and reproduction of root-knot nematode (RKN), Meloidogyne incognita was highest in BTH followed by SA and NA treatments. This was attributed to increased biosynthesis of CGA. The study firstly linked GSH and SA metabolism enhancing CGA biosynthesis in chickpea. The increase in CGA improved resistance against RKN. Seed treatment at 10.0 mu g/mL BTH 1 h before sowing is recommended as strategic management decision to contain RKN on chickpea.