Background: Arsenic (As) is a toxic metalloid for plant growth while wilt caused by Fusarium is a major yield-limiting factor in grain legumes. Despite immense threat of escalation of major biotic stresses in crops due to contaminated soil, the intrinsic cellular responses to Fusarium wilt under As exposure is not known. Furthermore, the role of primary antioxidant defense other than phenylpropanoid pathway in response to wilt is poorly understood in crop plants.
Methods: Effect of As on wilt tolerance was studied on four genotypes of grass pea (Lathyrus sativus L.) (30 days after commencement of treatment) in a controlled pot experiment with randomized block design in four replicates per four treatment: control (no Fusarium-inoculums, no As in soil), inoculums-treated soil and As + inoculums-treated soil. Data were statistically analyzed at a significant level of P < 0.05.
Results: In inoculums-treated soil, glutathione (GSH)-deficient gshL-1 mutant wilted but wilting symptom was conspicuously absent in variety BioL-212, ascorbate (AsA)-deficient mutant (asfL-1), and GSH-overproducing mutant. In presence of As, wilting symptoms appeared in BioL-212 and their severity increased in the gshL-1 mutant. Normal activity of phenylalanine ammonia-lyase (PAL) in susceptible gshL-1 mutant and remarkable tolerance of asfL-1 mutant to wilt despite low PAL activity, during As exposure, indicated involvement of antioxidant defense other than PAL in governing wilt sensitivity. Enhanced peroxidase level along with high GSH-redox and low ascorbate peroxidase activity tightly regulated H2O2 concentration and metabolism in fine tune, effectively preventing oxidative damage of membrane and concomitant escalation of wilting symptom. Low H2O2 level and deficient peroxidase activity, presumably, weakened gshL-1 defense against fungal invasion. By contrast, under As + inoculums-treated soils, H2O2 level reached toxic concentration in the mutant and also in variety BioL-212 resulting in onset of oxidative stress and appearance of wilting symptom in the severest form.
Conclusions: As has profound effect on PAL activity and induced/increased wilt symptom through modulation of H2O2 metabolism within AsA-GSH cycle and outside it. H2O2 level was found critical in determining tolerance or sensitivity of genotypes to Fusarium wilt, and the GSH-redox state holds the key to manage oxidative damage during pathogenic infection.
Keywords: Fusarium wilt, arsenic, phenylalanine ammonia-lyase, AsA-GSH cycle, redox state, peroxidase, H2O2, Lathyrus sativus L