Over-expression of Trxo1 and cell viability under H2O2 stress

Ortiz-Espín et al. treat over-expressing PsTrxo1 tobacco (Nicotiana tabacum) BY-2 cells with H2O2 and find a significant delay in cell death compared to controls, which may in part be due to a decreased content of endogenous H2O2 in the over-expressing cells, in which changes in oxidative parameters and antioxidants are less extended after the oxidative treatment.

Reactive oxygen species (ROS), especially hydrogen peroxide, play a critical role in the regulation of plant development and in the induction of plant defence responses during stress adaptation, as well as in plant cell death. The antioxidant system is responsible for controlling ROS levels in these processes but redox homeostasis is also a key factor in plant cell metabolism under normal and stress situations. Thioredoxins (Trxs) are ubiquitous small proteins found in different cell compartments, including mitochondria and nuclei (Trxo1), and are involved in the regulation of target proteins through reduction of disulphide bonds, although their role under oxidative stress has been less well studied.

Role of PsTrxo1 in TBY-2 cell death after treatment with 35 mM H2O2.
Role of PsTrxo1 in TBY-2 cell death after treatment with 35 mM H2O2. Full details in Ortiz-Espín et al.

Ortiz-Espín et al. treat over-expressing PsTrxo1 tobacco (Nicotiana tabacum) BY-2 cells with H2O2 and find a significant delay in cell death compared to controls, which may in part be due to a decreased content of endogenous H2O2 in the over-expressing cells, in which changes in oxidative parameters and antioxidants are less extended after the oxidative treatment. They conclude that PsTrxo1 transformation protects TBY-2 cells from exogenous H2O2, thus increasing their viability via a process in which not only antioxidants but also Trxo1 seem to be involved.

This article appears in the special issue ROS and NO Reactions in Plants.