Overexpression of soybean R2R3-MYB transcription factor, GmMYB12B2, and tolerance to UV radiation and salt stress in transgenic Arabidopsis.

MYB, v-myb avian myeloblastosis viral oncogene homolog, proteins play central roles in plant stress response. Previously, we identified a novel R2R3-MYB transcription factor, GmMYB12B2, which affected the expression levels of some key enzyme genes involved in flavonoid biosynthesis in transgenic Arabidopsis. In the present study, we analyzed the expression levels of GmMYB12B2 under salt, low temperature, drought, abscisic acid (ABA), and ultraviolet (UV) radiation treatments in soybean using semi-quantitative reverse transcription polymerase chain reaction. The expression of GmMYB12B2 was drastically induced by UV irradiation and salt treatment, but no response was detected under low temperature, drought, and ABA stresses. A detailed characterization of the GmMYB12B2 overexpression lines revealed that GmMYB12B2 might be involved in response of plants to UV radiation and salt stresses. Transgenic Arabidopsis lines constitutively expressing GmMYB12B2 showed an increased tolerance to salt and UV radiation treatment compared with wild-type plants. The expression levels of certain salt stress-responsive genes, such as DREB2A and RD17, were found to be elevated in the transgenic plants. These results indicate that GmMYB12B2 acts as a regulator in the plant stress response.

Stem cell factor protects against neuronal apoptosis by activating AKT/ERK in diabetic mice

Neuronal apoptosis occurs in the diabetic brain due to insulin deficiency or insulin resistance, both of which reduce the expression of stem cell factor (SCF). We investigated the possible involvement of the activation of the MAPK/ERK and/or AKT pathways in neuroprotection by SCF in diabetes. Male C57/B6 mice (20-25 g) were randomly divided into four groups of 10 animals each. The morphology of the diabetic brain in mice treated or not with insulin or SCF was evaluated by H&E staining and TUNEL. SCF, ERK1/2 and AKT were measured by Western blotting. In diabetic mice treated with insulin or SCF, there was fewer structural change and apoptosis in the cortex compared to untreated mice. The apoptosis rate of the normal group, the diabetic group receiving vehicle, the diabetic group treated with insulin, and the diabetic group treated with SCF was 0.54 ± 0.077 percent, 2.83 ± 0.156 percent, 1.86 ± 0.094 percent, and 1.78 ± 0.095 percent (mean ± SEM), respectively. SCF expression was lower in the diabetic cortex than in the normal cortex; however, insulin increased the expression of SCF in the diabetic cortex. Furthermore, expression of phosphorylated ERK1/2 and AKT was decreased in the diabetic cortex compared to the normal cortex. However, insulin or SCF could activate the phosphorylation of ERK1/2 and AKT in the diabetic cortex. The results suggest that SCF may protect the brain from apoptosis in diabetes and that the mechanism of this protection may, at least in part, involve activation of the ERK1/2 and AKT pathways. These results provide insight into the mechanisms by which SCF and insulin exert their neuroprotective effects in the diabetic brain.

Stem cell factor protects against neuronal apoptosis by activating AKT/ERK in diabetic mice.

Neuronal apoptosis occurs in the diabetic brain due to insulin deficiency or insulin resistance, both of which reduce the expression of stem cell factor (SCF). We investigated the possible involvement of the activation of the MAPK/ERK and/or AKT pathways in neuroprotection by SCF in diabetes. Male C57/B6 mice (20-25 g) were randomly divided into four groups of 10 animals each. The morphology of the diabetic brain in mice treated or not with insulin or SCF was evaluated by H&E staining and TUNEL. SCF, ERK1/2 and AKT were measured by Western blotting. In diabetic mice treated with insulin or SCF, there was fewer structural change and apoptosis in the cortex compared to untreated mice. The apoptosis rate of the normal group, the diabetic group receiving vehicle, the diabetic group treated with insulin, and the diabetic group treated with SCF was 0.54 +/- 0.077%, 2.83 +/- 0.156%, 1.86 +/- 0.094%, and 1.78 +/- 0.095% (mean +/- SEM), respectively. SCF expression was lower in the diabetic cortex than in the normal cortex; however, insulin increased the expression of SCF in the diabetic cortex. Furthermore, expression of phosphorylated ERK1/2 and AKT was decreased in the diabetic cortex compared to the normal cortex. However, insulin or SCF could activate the phosphorylation of ERK1/2 and AKT in the diabetic cortex. The results suggest that SCF may protect the brain from apoptosis in diabetes and that the mechanism of this protection may, at least in part, involve activation of the ERK1/2 and AKT pathways. These results provide insight into the mechanisms by which SCF and insulin exert their neuroprotective effects in the diabetic brain.