Department of Biotechnology, St. Xavier's College (Autonomous), 30, Mother Teresa Sarani, Kolkata, 700016, West Bengal, India.
Protoplasma. 2022 Sep;259(5):1331-1350. doi: 10.1007/s00709-022-01740-7. Epub 2022 Jan 27.
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.
本研究旨在探讨脱落酸（ABA）是否像诱导水稻适应盐胁迫一样促进氟化物耐受。将三种耐盐水稻基因型的种子在光照/黑暗光周期为 16/8 h、光照强度为 700 μmol 光子 m-2 s-1 和相对湿度为 50%的植物生长室中于 32°C下保持 20 天。抑制 ABA 生物合成和下调 ABA 诱导基因如 Rab16A、Osem 和 TRAB1 的表达，导致 NaCl 诱导的生长抑制和生理损伤，如叶绿素降解、电解质渗漏、HO 的形成、丙二醛和甲基乙二醛在 Matla 中的形成。ABA 积累减少增加了 NaF（50 mg L-1）胁迫下 Nonabokra 和 Matla 中褪黑素和赤霉素的水平，这共同促进了氟化物耐受。在 NaF 胁迫下，Jarava 中较高的 ABA 含量通过氯离子通道刺激氟化物摄取，从而表现出严重的氟化物敏感性，尽管通过 PDH、ADC、ODC、SAMDC、SPDS、SPMS、DAO 和 PAO 等基因的协同作用，产生了更多与 ABA 相关的渗透物，如脯氨酸、甘氨酸甜菜碱和多胺。在高内源性 ABA 存在下，相容性溶质的积累增加促进了 Jarava 的耐盐性；但这不足以改善该品种中由氟化物引起的损伤。ABA 生物合成抑制剂 NaWO 的处理促进了 Jarava 的氟化物耐受性，而外源 ABA 的进一步补充则导致其恢复到氟化物敏感表型。我们的工作清楚地表明，ABA 不能总是被认为是文献中已知的“通用”应激激素，因为它作为氟化物耐受性的负调节剂，在水稻中通过与 ABA 无关的褪黑素和赤霉素依赖途径更紧密地调节。
