Long-term treatments with microcystin-LR and diquat reveal their differences in the induction of oxidative stress responses and mitotic alterations in terms of stress recovery in Arabidopsis roots.

Microcystin-LR (MCY-LR), a widespread natural cyanobacterial toxin is a potent inhibitor of type 1 and 2A protein phosphatases (PP1, PP2A), inducing oxidative stress as well. Diquat (DQ) is a herbicide that inhibits electron transport to induce strong oxidative stress. Both compounds are affecting natural environments as well as plant and human health. We conducted a comparative analysis on their long-term (48 h) effects on reactive oxygen species (ROS) production, mitosis and histone H3 phosphorylation in root apical meristems of wild-type and PP2A-related mutants of Arabidopsis thaliana. MCY-LR did not increase ROS levels in any of the genotypes, but increased significantly the activity of ROS scavenging peroxidases (PODs) in Col0. DQ decreased ROS levels, but did not affect PODs. The paradoxical effect of DQ indicated the initiation of cell death processes. Mitosis was not affected by MCY-LR, but inhibited by DQ. Interestingly, MCY-LR as a phosphatase inhibitor did not affect histone H3 phosphorylation in mitotic cells, but DQ had an increasing effect. As we have shown previously, most of the above parameters changed differently at shorter (24 h) exposures: both compounds increased ROS levels in the phosphatase mutants, while POD activities were not affected; inhibition of mitosis or arrests in early mitosis, as well as increases of histone H3 phosphorylation levels occurred in the presence of both compounds. To conclude, Arabidopsis is able of recover partially and transiently from MCY-LR induced stress at long-term exposure, but this is not true for DQ. The environmental relevance of these findings is discussed.