4.7 Article

Methyl jasmonate alleviates arsenic toxicity in rice

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PLANT CELL REPORTS
卷 39, 期 8, 页码 1041-1060

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SPRINGER
DOI: 10.1007/s00299-020-02547-7

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Arsenic; Rice; Methyl jasmonate; Oxidative stress; Arsenic transporters; Fe transporters

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Key message Methyl jasmonate improved yield of both rice varieties under arsenic toxicity by alleviating oxidative stress through increasing the activity of antioxidant enzymes and decreasing arsenic accumulation by modulating arsenic transporters. Human health and rice cultivation are threatened by arsenic (As) contamination. Methyl jasmonate (MJ), as a regulator of plant growth, plays an important role in response to environmental stresses. In the present study, the effects of MJ (0, 0.5 and 1 mu M) on yield, biochemical and molecular traits of two rice varieties (T. hashemi and Fajr) under As treatments (0, 25 and 50 mu M) were investigated. The results showed that As decreased chlorophyll content, chlorophyll fluorescence and biomass production; however, MJ improved photosynthetic pigments and plant growth. As also induced oxidative stress (H2O2 and MDA) in both rice varieties; however, MJ reduced the As-induced oxidative stress by regulating the activity of antioxidant enzymes and the ASA-GSH cycle. As treatment increased As accumulation in the roots and leaves, which is in line with the increased expression of Lsi1, Lsi2 and Lsi6 genes. However, MJ reduced As accumulation by decreasing the expression of Lsi1, Lsi2 and Lsi6. Fe translocation to leaves reduced under As treatments; while, MJ increased Fe accumulation in the leaves by increasing expression of FRDL1 and YSL2 transporters under As toxicity. As treatments, especially 50 mu M, decreased yield and yield components of both rice varieties; however, MJ improved yield and yield components of both rice varieties. The findings of the present study indicate that MJ improved the growth and yield of both rice varieties under As toxicity by alleviating oxidative stress through increasing the activity of antioxidant enzymes and ASA-GSH cycle and decreasing As accumulation by modulating As transporters.

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