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Coordinated response of sulfate transport, cysteine biosynthesis, and glutathione-mediated antioxidant defense in lentil (Lens culinaris Medik.) genotypes exposed to arsenic
D TALUKDAR
Published in Springer-Verlag Wien
2014
Volume: 251
   
Issue: 4
Pages: 839 - 855
Abstract
Response of sulfate transporters, thiol metabolism, and antioxidant defense system was studied in roots of two lentil (Lens culinaris Medik.) genotypes grown in arsenic (10, 25, and 40 μM AsV)-supplemented nutrient solution, and significant changes compared to control (0 μM AsV) were observed mainly at 25 and 40 μM. In L 414, high glutathione (GSH) redox (0.8-0.9) was maintained with elevated thiol synthesis, powered by transcriptional up-regulation of LcSultr1;1 and LcSultr1;2 sulfate transporters and significant induction of LcSAT1;1 and LcSAT1;2 (serine acetyltransferase), OAS-TL (O-acetylserine(thiol)-lyase), γ-ECS (γ-glutamylcysteine synthetase), and PCS (phytochelatin synthase) genes predominantly within 12-24 h of As exposure at 25 μM and within 6-12 h at 40 μM. This thiolic potency in L 414 roots was effectively complemented by up-regulation of gene expressions and consequent enhanced activities of superoxide dismutase, ascorbate peroxidase (APX), dehydroascorbate reductase, glutathione reductase (GR), and glutathione-S-transferase (GST) isoforms at 25 and 40 μMAs, efficiently scavenging excess reactive oxygen species to prevent onset of As-induced oxidative stress and consequent inhibition of root growth in L 414. In contrast, down-regulation of vital sulfate-uptake transporters as well as entire thiol-metabolizing system and considerably low APX, GST, and GR expressions in DPL 59 not only resulted in reduced GSH redox but also led to over-accumulation of H2O2. This triggered membrane lipid peroxidations as the marks of As-induced oxidative damage. Results indicated coordinated response of thiol-metabolism and antioxidant defense in conferring As-tolerance in lentil, and GSH is the key point in this cascade. © 2013 Springer-Verlag Wien.
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JournalData powered by TypesetProtoplasma
PublisherData powered by TypesetSpringer-Verlag Wien
ISSN0033-183X