Upregulation of genes encoding plastidic isoforms of antioxidant enzymes and osmolyte synthesis impart tissue tolerance to salinity stress in bread wheat

Wheat genotype Kharchia is a donor for salt tolerance in wheat breeding programs worldwide; however, the tolerance mechanism in Kharchia is yet to be deciphered completely. To avoid spending energy on accumulating organic osmolytes and to conserve resources for maintaining growth, plants deploy sodium (Na+) ions to maintain turgor. The enhanced ability to tolerate excess ion accumulation and ion toxicity is designated as tissue tolerance. In this study, salt-tolerant wheat genotype (Kharchia 65) and sensitive cultivars (HD2687, HD2009, WL711) were exposed to vegetative stage salinity stress (for four weeks). Kharchia 65 showed better tissue tolerance to salinity than the other genotypes based on different physiological parameters. Gene expression and abundance of chloroplast localized antioxidant enzymes and compatible osmolyte synthesis were upregulated by salinity in Kharchia 65. In Kharchia 65, the higher abundance of NADPH Oxidase (RBOH) transcripts and localization of reactive oxygen species (ROS) suggested an apoplastic ROS burst. Expression of calcium signaling genes of SOS pathway, MAPK6, bZIP6 and NAC4 were also upregulated by salinity in Kharchia 65. Considering that Kharchia local is the donor of salt tolerance trait in Kharchia 65, the publically available Kharchia local transcriptome data were analyzed. Our results and the in-silico transcriptome analysis also confirmed that higher basal levels and the stress-induced rise in the expression of plastidic isoforms of antioxidant enzymes and osmolyte biosynthesis genes provide tissue tolerance in Kharchia 65. Thus, in salinity tolerant genotype Kharchia 65, ROS burst mediated triggering of calcium signaling improves Na+ exclusion and tissue tolerance to Na+.