Active ingredient of the commercial herbicide BASTA (B), phosphinothricin, acts as an inhibitor of glutamine synthetase (GS), a key enzyme in ammonium assimilation. The treatment with BASTA leads to an elevation of ammonium levels in plants and further to various physiological alterations, ammonium toxicity and lethality. Results of the present study emphasize the complexity underlying control mechanisms that determine BASTA interaction with essential oil (EO) from Nepeta rtanjensis (NrEO), bioherbicide inducing oxidative stress in target plants. Simultaneous application of NrEO and BASTA, two agents showing differential mode of action, suspends BASTA-induced ammonium toxicity in Arabidopsis thaliana plants. This is achieved through maintaining GS activity, which sustains a sub-toxic and/or sub-lethal ammonium concentration in tissues. As revealed by the present study, regulation of GS activity, as influenced by BASTA and NrEO, occurs at transcriptional, posttranscriptional, and/or posttranslational levels. Two genes encoding cytosolic GS, GLN1;1 and GLN1;3, are highlighted as the main isozymes in Arabidopsis shoots contributing to NrEO-induced overcoming of BASTA-generated ammonium toxicity. The effects of NrEO might be ascribed to its major component nepetalactone, but the contribution of minor EO components should not be neglected. Although of fundamental significance, the results of the present study suggest possible low efficiency of BASTA in plantations of medicinal/aromatic plants such as Nepeta species. Furthermore, these results highlight the possibility of using NrEO as a bioherbicide in BASTA-treated crop fields to mitigate the effect of BASTA residues in contaminated soils.
Keywords: Ammonium toxicity; Arabidopsis; Essential oil; Glutamine synthetase; Nepeta; Phosphinothricin.
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