Breeding of Penta Null Soybean [Glycine max (L.) Merr.] for Five Antinutritional and Allergenic Components of Lipoxygenase, KTI, Lectin, 7S α' Subunit, and Stachyose.

Soybean [Glycine max (L.) Merr.] is an excellent source of protein, oil, carbohydrates and many other bioactive ingredients for humans. However, several antinutritional and allergenic components such as lipoxygenase, KTI, lectin, 7S α' subunit, and stachyose exist in the raw mature seed. Genetic removal of these components would be the best method to improve soybean food quality. The objectives of this research were to breed a new soybean line with penta null recessive alleles (lox1/lox1/lox2/lox2/lox3/lox3-ti/ti-le/le-cgy1/cgy1-rs2/rs2) for these five components and to evaluate agronomic traits for a breeding line with penta null alleles. Seven germplasms were used to breed the penta null strain. Analysis of lipoxygenase, KTI, lectin, 7S α' subunit, and stachyose components in mature seeds was conducted by SDS-PAGE, western blot, and HPLC. One breeding line with penta null recessive alleles was developed. The breeding line has purple flowers, tawny pubescence, a determinate growth habit, and light yellow pods at maturity. The seed of the breeding line has a yellow hilum and yellow seed coat color. The stem height of the breeding line was 53.0 cm. The stachyose content of the breeding line was 2.9 g/kg. The 100-seed weight of the breeding line was 31.1 g and yield (t/ha) was 2.80. This is the first soybean strain with the penta null (lox1lox2lox3/lox1lox2lox3-ti/ti-le/le-cgy1/cgy1-rs2/rs2) genotype (free of lipoxygenase, KTI, lectin, and 7S α' subunit proteins, and with low stachyose content).

Modulation by the GABA(B) receptor siRNA of ethanol-mediated PKA-α, CaMKII, and p-CREB intracellular signaling in prenatal rat hippocampal neurons.

Fetal alcohol syndrome (FAS) is a developmental neuropathology resulting from in utero exposure to ethanol; many of ethanol's effects are likely to be mediated by the neurotransmitter γ-aminobutyric acid (GABA). We studied modulation of the neurotransmitter receptor GABA(B)R and its capacity for intracellular signal transduction under conditions of ethanol treatment (ET) and RNA interference to investigate a potential role for GABA signaling in FAS. ET increased GABA(B1)R protein levels, but decreased protein kinase A-α (PKA-α), calcium/calmodulin-dependent protein kinase II (CaMKII) and phosphorylation of cAMP-response element binding protein (p-CREB), in cultured hippocampal neurons harvested at gestation day 17.5. To elucidate GABA(B1)R response to ethanol, we observed the effects of a GABA(B)R agonist and antagonist in pharmacotherapy for ethanol abuse. Baclofen increased GABA(B)R, CaMKII and p-CREB levels, whereas phaclofen decreased GABA(B)R, CaMKII and p-CREB levels except PKA-α. Furthermore, when GABA(B1)R was knocked down by siRNA treatment, CaMKII and p-CREB levels were reduced upon ET. We speculate that stimulation of GABA(B1)R activity by ET can modulate CaMKII and p-CREB signaling to detrimental effect on fetal brain development.