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Transgenic Brassica napus plants overexpressing aluminium‐induced mitochondrial manganese superoxide dismutase cDNA are resistant to aluminium
Author(s) -
Basu U.,
Good A. G.,
Taylor G. J.
Publication year - 2001
Publication title -
plant, cell and environment
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.646
H-Index - 200
eISSN - 1365-3040
pISSN - 0140-7791
DOI - 10.1046/j.0016-8025.2001.00783.x
Subject(s) - superoxide dismutase , malondialdehyde , canola , brassica , callose , transgene , biology , lipid peroxidation , genetically modified crops , reactive oxygen species , antioxidant , horticulture , biochemistry , botany , cell wall , gene
We investigated the role that manganese superoxide dismutase (MnSOD, EC 1·15·1·1), an important enzyme of the antioxidant pathway, may play in aluminium (Al) toxicity/resistance. A wheat ( Triticum aestivum ) cDNA ( WMnSOD ) was cloned and up‐regulation of the transcript was observed in root tips after 24 h exposure to 100 µ m Al. The WMnSOD1 under the control of the CaMV 35S promoter was expressed in canola ( Brassica napus ). Transgenic plants were phenotypically normal. Northern analyses showed enhanced levels of the WMnSOD1 and WMnSOD1‐GUS transcripts and total SOD activity was 1·5‐ to 2·5‐fold greater in transgenic plants than in wild type (WT) plants. Transgenic (T 1 ) leaf discs showed increased retention of chlorophyll and reduced electrolyte leakage when exposed to methyl viologen (MV) as compared with WT leaf discs, suggesting that transgenic plants were more resistant to oxidative stress. When WT canola plants were exposed to aluminium (0–200 µ m ), inhibition of root growth, higher SOD activity and increased levels of malondialdehyde (MDA, an indicator of lipid peroxidation) were observed in roots. Aluminium‐induced inhibition of root growth and accumulation of MDA was lower in homozygous transgenic plants (T 2 ) compared with WT plants. Transgenic lines also showed lower synthesis of 1,3‐ β ‐glucans (callose, a sensitive marker for Al injury) as compared with WT. These data suggest that resistance to Al toxicity can be improved by overexpressing WMnSOD1 .