Fluoride tolerance in rice is negatively regulated by the 'stress-phytohormone' abscisic acid (ABA), but promoted by ABA-antagonist growth regulators, melatonin, and gibberellic acid.

The present manuscript aimed at investigating whether abscisic acid (ABA) promotes fluoride tolerance, similar to inciting salt adaptation in rice. Seeds of three salt-tolerant rice genotypes were maintained at 32 °C under 16/8 h light/dark photoperiodic cycle with 700 μmol photons m s intensity and 50% relative humidity in a plant growth chamber for 20 days. Suppressed ABA biosynthesis, and downregulated expression of ABA-inducible genes like Rab16A, Osem, and TRAB1 triggered NaCl-induced growth inhibition and physiological injuries like chlorophyll degradation, electrolyte leakage, formation of HO, malondialdehyde, and methylglyoxal in Matla. Reduced ABA accumulation increased the levels of melatonin and gibberellic acid in NaF (50 mg L)-stressed Nonabokra and Matla, which altogether promoted fluoride tolerance. Higher ABA content in NaF-stressed Jarava stimulated fluoride uptake via chloride channels, thus exhibiting severe fluoride susceptibility, in spite of higher production of ABA-associated osmolytes like proline, glycine-betaine and polyamines via the concerted action of genes like PDH, ADC, ODC, SAMDC, SPDS, SPMS, DAO, and PAO. Increased accumulation of compatible solutes in presence of high endogenous ABA promoted salt tolerance in Jarava; the same was insufficient to ameliorate fluoride-induced injuries in this cultivar. Treatment with ABA biosynthetic inhibitor, NaWO promoted fluoride tolerance in Jarava, whereas further supplementation with exogenous ABA resulted in reversion back to fluoride-susceptible phenotype. Our work clearly established that ABA cannot always be considered as a 'universal' stress hormone as known in literature, since it acts as a negative regulator of fluoride tolerance which is more tightly regulated in rice via melatonin- and gibberellic acid-dependent pathways in ABA-independent manner.