The glutamate dehydrogenase gene gdhA increased the resistance of tobacco to glufosinate

Authors: S A Nolte; B G Young; R Mungur; D A Lightfoot

Source: Weed Research, Volume 44, Number 4, August 2004 , pp. 335-339(5)

Publisher: Wiley-Blackwell

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Abstract:

Summary

The gene gdhA from Escherichia coli, that encodes a NADPH-dependent glutamate dehydrogenase (GDH), directs a novel pathway in transgenic plants that allows an increase in ammonium assimilation. Glufosinate leads to plant death by the irreversible inhibition of glutamate synthetase (GS) leading to a disruption of subsequent GS-related processes resulting in elevated ammonium and disruption of photorespiration. Therefore, it was speculated that the gdhA-transformed plants may exhibit a novel mechanism of resistance to glufosinate by altered activity of the GDH-directed pathway(s) and subsequently related processes. Studies were conducted in the greenhouse to evaluate the resistance of tobacco plants containing the gdhA gene to glufosinate. Five tobacco genotype lines were investigated including a non-transformed control line, a positive control line and three transformed lines with levels of increasing GDH activity directed by the gdhA gene. Plants transformed with the gdhA gene expressed up to six times increased level of resistance (GR50) to glufosinate compared with the non-transformed control, which is 100 times less resistant than plants transformed with the bar gene. The GDH activity among lines was highly correlated (r2 = 0.9903) with the level of herbicide resistance. Thus, the use of the E. coli gdhA gene in plant transformations can provide an additional mechanism for resistance to glufosinate.

Keywords: gdhA; glufosinate resistance; glutamate dehydrogenase; glutamine synthetase; plant transformation; tobacco; Nicotiniana tabacum

Document Type: Research article

DOI: http://dx.doi.org/10.1111/j.1365-3180.2004.00411.x

Affiliations: 1: Department of Plant, Soil, and Agricultural Systems, Southern Illinois University, Carbondale, IL, USA

Publication date: 2004-08-01

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