NADPH-dependent thioredoxin reductase A (NTRA) confers elevated tolerance to oxidative stress and drought
- PMID: 24792388
- DOI: 10.1016/j.plaphy.2014.04.008
NADPH-dependent thioredoxin reductase A (NTRA) confers elevated tolerance to oxidative stress and drought
Abstract
NADPH-dependent thioredoxin reductases (NTRs) are key-regulatory enzymes determining the redox state of the thioredoxin (Trx) system that provides reducing power to peroxidases or oxidoreductases. Moreover, it also plays an essential function in the direct reduction of ROS and acquiring stress tolerance in plant. Cytoplasmic NTRA, mitochondrial NTRB, and chloroplastic NTRC are the three conserved NTRs which cooperate with specific sub-cellularly localized Trxs in Arabidopsis. However, cytosolic NTRs such as NTRA in Arabidopsis have not previously been identified in plants or mammals as a source of functional redundancy with mitochondrial NTRs. Here, we show the involvement of NTRA in the plant stress response counteracting oxidative and drought stresses. Methyl viologen (MV), an inducer of oxidative stress in plants, enhanced the NTRA transcripts. To identify the physiological role of NTRA influencing ROS homeostasis by stress, NTRA overexpression (NTRAOX) and knock-out mutants (ntra-ko) were generated. After exposure to oxidative stress, wild-type and ntra-ko plants were sensitive, but NTRAOX plants tolerant. ROS range was increased by MV in wild-type and ntra-ko plants, but not in NTRAOX. Investigating the involvement of Arabidopsis NTRA in drought, NTRAOX plants exhibited extreme drought tolerance with high survival rates, lower water loss and reduced ROS compared to wild-type and ntra-ko plants. Transcripts of drought-responsive genes, such as RD29A and DREB2A, were highly expressed under drought and antioxidant genes, namely CuZnSOD and APX1 were enhanced in the absence of drought in NTRAOX plants. The results suggest that NTRA overexpression confers oxidative and drought tolerance by regulation of ROS amounts.
Keywords: Antioxidant; Drought stress; NADPH-dependent thioredoxin reductase A; Oxidative stress; Reactive oxygen species; Water deficit.
Copyright © 2014 Elsevier Masson SAS. All rights reserved.
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