Strigolactones Modulate Cellular Antioxidant Defense Mechanisms to Mitigate Arsenate Toxicity in Rice Shoots

Metalloid contamination, such as arsenic poisoning, poses a significant environmental problem, reducing plant productivity and putting human health at risk. Phytohormones are known to regulate arsenic stress; however, the function of strigolactones (SLs) in arsenic stress tolerance in rice is rarely investigated. Here, we investigated shoot responses of wild-type (WT) and SL-deficient d10 and d17 rice mutants under arsenate stress to elucidate SLs’ roles in rice adaptation to arsenic. Under arsenate stress, the d10 and d17 mutants displayed severe growth abnormalities, including phenotypic aberrations, chlorosis and biomass loss, relative to WT. Arsenate stress activated the SL-biosynthetic pathway by enhancing the expression of SL-biosynthetic genes D10 and D17 in WT shoots. No differences in arsenic levels between WT and SL-biosynthetic mutants were found from Inductively Coupled Plasma-Mass Spectrometry analysis, demonstrating that the greater growth defects of mutant plants did not result from accumulated arsenic in shoots. The d10 and d17 plants had higher levels of reactive oxygen species, water loss, electrolyte leakage and membrane damage but lower activities of superoxide dismutase, ascorbate peroxidase, glutathione peroxidase and glutathione S-transferase than did the WT, implying that arsenate caused substantial oxidative stress in the SL mutants. Furthermore, WT plants had higher glutathione (GSH) contents and transcript levels of OsGSH1, OsGSH2, OsPCS1 and OsABCC1 in their shoots, indicating an upregulation of GSH-assisted arsenic sequestration into vacuoles. We conclude that arsenate stress activated SL biosynthesis, which led to enhanced arsenate tolerance through the stimulation of cellular antioxidant defense systems and vacuolar sequestration of arsenic, suggesting a novel role for SLs in rice adaptation to arsenic stress. Our findings have significant implications in the development of arsenic-resistant rice varieties for safe and sustainable rice production in arsenic-polluted soils.

Neither glutamate nor alanine but arginine sensitizes BY-2 cells to arsenate

Arsenic is toxic for plants. Our previous results showed that the application of proline enhanced the sensitivity of tobacco BY-2 cells to arsenate. In order to clarify the enhancement mechanism, we investigated the effects of other amino acids on the arsenate-stressed BY-2 cells. Glutamate at up to 10 mM did not affect the cell growth in the absence or presence of arsenate. Arginine at up to 10 mM did not affect the growth in the absence of arsenate but arginine at 10 mM enhanced the inhibition of the cell growth by arsenate. Alanine at up to 10 mM did not affect the cell growth under non-stressed condition but alanine at 10 mM significantly improved the cell growth under arsenate stress. These results suggest that alanine mitigates arsenate stress in BY-2 cells and that arginine like proline enhances the sensitivity of BY-2 cells to arsenate.

Silicon induces adventitious root formation in rice (Oryza sativa L.) under arsenate stress with the involvement of nitric oxide and indole-3-acetic acid

Arsenic (As) negatively affects plant development. Using rice as a model, this study evaluates how the application of silicon (10 µM Si) can favour the formation of adventitious roots under arsenate stress (50 µM As V) as a mechanism to mitigate its negative effects. Indeed, the simultaneous application of As V and Si up-regulated the expression of genes involved in nitric oxide (NO) metabolism (OsNOA1), cell cycle progression (G2-M, OsCDKA1), auxin (IAA, indole-3-acetic acid) biosynthesis (OsYUCCA1 and OsTAA1) and transport (OsPIN1, OsPIN5 and OsPIN10) and Si uptake (OsLsi1 and OsLsi2), which accompanied adventitious root formation. Furthermore, Si triggered the expression and activity of MDHAR and DHAR involved in ascorbate recycling. The treatment with L-NAME, an inhibitor of NO generation, significantly suppressed adventitious root formation, even in the presence of Si; however, supplying NO in the growth media rescued its effects. The data obtained suggest that both NO and IAA are essential for Si-mediated adventitious root formation under As V stress. Interestingly, TIBA (a polar auxin transport inhibitor) suppressed adventitious root formation, even in the presence of Si and SNP (an NO donor), suggesting that Si is involved in a mechanism whereby a cellular signal is triggered and requires NO formation first and, then, IAA.