A bentazone-resistant mutant of cyanobacterium, Synechococcus elongatus PCC7942 adapts different strategies to counteract on bromoxynil- and salt-mediated oxidative stress.

A bentazone-resistant mutant of Synechococcus elongatus PCC7942, called Mu2, tolerated elevated NaCl concentrations. As bentazone and bromoxynil exhibit similar mechanism of action, we investigated whether the mutant also toleratedbromoxynil and found it to be true. The line of investigation was then whether the acclimation strategy for the three stressors, bentazone, bromoxynil and NaCl was same or different. The cellular contents of malondialdehyde, hydrogen peroxide and superoxide increased in wild type strain following all the treatments suggesting their toxicities due to oxidative response. Notwithstanding, there were apparently different anti-oxidative measures pertaining to the herbicide and salinity stress. Glutathione contents and activities of superoxide dismutase, catalase-peroxidase, glutathione S-transferase and glutathione reductase decreased under NaCl, whereas bromoxynil affected only glutathione S-transferase reductase. Moreover, in-gel assays revealed that bromoxynil promoted appearance of isozymes of catalase-peroxidase, while NaCl induced such response only for superoxide dismutase. On the other hand, in Mu2, glutathione peroxidase-reductase and glutathione showed upward trend after bromoxynil exposure, whereas NaCl raised peroxidase and superoxide dismutase. Proteome comparison revealed peroxiredoxin Q to be highly expressed in wild type strain under bromoxynil, whereas NaCl favoured flavodoxin over-expression. Their amounts were already high in Mu2. We suggest that Mu2 acclimatized to bromoxynil in a manner similar to bentazone by upgrading peroxiredoxin Q and glutathione peroxidase-reductase. Conversely, for NaCl it devised another mechanism involving peroxidase and superoxide dismutase, and flavodoxin.