We constructed two series of Gateway binary vectors, pGWBs and R4pGWBs, possessing the bialaphos resistance gene (bar) as a selection marker for plant transformation. The reporters and tags employed in this system are sGFP, GUS, LUC, EYFP, ECFP, G3GFP, mRFP, TagRFP, 6xHis, FLAG, 3xHA, 4xMyc, 10xMyc, GST, T7 and TAP. Selection of Arabidopsis transformants with BASTA was successfully carried out using both plate-grown and soil-grown seedlings. Transformed rice calli and suspension-cultured tobacco cells were selected on plates containing BASTA or glufosinate-ammonium. These vectors are compatible with existing pGWB and R4pGWB vectors carrying kanamycin and hygromycin B resistance.

Plants use sophisticated strategies to balance responses to oxidative stress. Programmed cell death, including the hypersensitive response (HR) associated with successful pathogen recognition, is one cellular response regulated by reactive oxygen in various cellular contexts. The Arabidopsis basic leucine zipper (bZIP) transcription factor AtbZIP10 shuttles between the nucleus and the cytoplasm and binds consensus G‐ and C‐box DNA sequences. Surprisingly, AtbZIP10 can be retained outside the nucleus by LSD1, a protein that protects Arabidopsis cells from death in the face of oxidative stress signals. We demonstrate that AtbZIP10 is a positive mediator of the uncontrolled cell death observed in lsd1 mutants. AtbZIP10 and LSD1 act antagonistically in both pathogen‐induced HR and basal defense responses. LSD1 likely functions as a cellular hub, where its interaction with AtbZIP10 and additional, as yet unidentified, proteins contributes significantly to plant oxidative stress responses.

The oxidative stress response of rice cytosolic ascorbate peroxidase (APX) was examined. The transcript level of cytosolic APX was significantly increased when suspension cultures of germinating rice embryos were treated with paraquat (7.9-fold) or H₂O₂ (6.1-fold). Induction by paraquat reached a maximum at 8 h. Induction by H₂O₂ peaked earlier at 4 h of treatment. This result suggests that the induction by paraquat might be caused by the H₂O₂ generated from superoxide. Treatment with a superoxide dismutase inhibitor, diethyldithiocarbamate, which is supposed to decrease the cellular H₂O₂ level, reduced the paraquat induction of cytosolic APX. In contrast, when APX and catalase were inhibited by hydroxyurea or aminotriazole, cellular H₂O₂ content was elevated and cytosolic APX mRNA was markedly increased without paraquat or H₂O₂ treatment. This suggests that cytosolic APX is regulated by the H level within cells. An increase in H₂O₂ content was observed in the paraquat treated embryos, suggesting that paraquat induction of cytosolic APX was caused by H₂O₂ generated through superoxide dismutation. These results indicate that H₂O₂ is involved in oxidative stress signalling, leading to the induction of cytosolic APX.