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BackgroundMimosa pigra is an invasive weed in some regions of South East Asia and Australia. Our previous study has revealed that a cyanobacterium, Nostoc sp., extract can inhibit root growth in M. pigra seedlings. In this study, some physiological processes involve oxidative stress-mediated cell death and root ultrastructure were investigated to clarify the mechanisms of root growth suppression and bioherbicidal potential of the extract.ResultsNostoc sp. extract enhanced overproduction of reactive oxygen species (ROS) at 24 h, the intensity of red fluorescence increased at 72 h, and caused a slightly increased H2O2 consistent with the activation of scavenging enzymes (catalase, ascorbic acid peroxidase, glutathione reductase, and peroxidases). This suggests that oxidative stress occurred in the presence of the extract which was supported by increased cell death and lipid peroxidation at 24 h. Reduction of malondialdehyde content and an increase in cell death at 72 h indicated oxidative damage and cellular leakage. Ultrastructural changes were determined at 72 h by scanning electron micrographs which confirmed the damage of epidermal and root cap cells and the disaggregation and destruction of root tip cells. Transmission electron micrographs showed the dissolution of the middle lamella, deposition of some substances in vacuoles, and abnormal mitochondria (swollen mitochondria and indistinct cristae).ConclusionsNostoc sp. extract enhance oxidative stress by ROS production resulting in lipid peroxidation and massive cell death despite the activation of antioxidative enzymes. Understanding mechanism of action of Nostoc sp. extract will provide information for application of the extract to use as natural herbicide for control of M. pigra.Electronic supplementary materialThe online version of this article (doi:10.1186/s40529-014-0081-3) contains supplementary material, which is available to authorized users.

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Vetiver (Vetiveria zizanioides Nash) cells derived from an inflorescence were cultured in a modified N6 liquid medium supplemented with 10 µm 2,4‐D and 10 mm proline. Exponentially growing cell suspensions were subcultured with a selection medium containing glufosinate (ammonium dl‐homoalanin‐4‐yl(methyl)phosphinate). The glufosinate‐resistant cells which can grow in a medium containing 5 × 10−5 M glufosinate was selected by a stepwise selection, and its I50 value was determined to be 4.2 × 10−5 M. The growth of susceptible cells was inhibited by lower concentrations of glufosinate and its I50 value was 2.5 × 10−7 M. This indicated that the selected cells were 170‐fold resistant compared with the susceptible cells. Glutamine synthetase (GS) activity of the resistant cells was twice as high as that of the susceptible cells. The I50 values of glufosinate were 3.2 × 10−5 M and 9.0 × 10−7 M for GS from the resistant and susceptible cells, respectively. The accumulation of ammonia caused by GS inhibition was higher in the susceptible cells. Absorption of [3,4–14C]glufosinate was not significantly different between the resistant and susceptible cells. Both cell types did not metabolize glufosinate. These results suggest that the resistance of the selected vetiver cell suspension to glufosinate is mainly due to increased GS activity and its decreased sensitivity to the herbicide.