Role of N2-fixation in the sustainability of the ponded grass pasture system

Ponded pastures in northern Australia produce green fodder in the seasonally dry winter period and may be employed to reduce grazing pressure on dryland pastures. The soils under ponded pasture, currently 26,000 ha in Queensland, are inherently infertile. This study was conducted to determine if a non-symbiotic association between bacteria and grass roots was responsible for the supply of N to ponded grasses. Intact soil-plant cores were obtained from a new ponded pasture of Aleman (Echinochloa polystachya) and an 8-year-old pasture of Hymenachne (Hymenachne amplexicaulis). Nitrogenase (N2-ase) activity was measured using the acetylene reduction assay and bacteria were selectively isolated to N-free malate medium from root segments of the most active plants. N2-ase activity of the intact soil-plant cores ranged from 76 to 380 g N ha−1 d−1 for the Aleman pasture and from 5 to 179 g N ha−1 d−1 for the Hymenachne pasture. Assays on excised roots showed the greatest activity on adventitious roots formed on the submerged nodes of Hymenachne stems. No major differences in colony morphology were detected in N2-fixing bacteria isolated from the roots of the two grasses. An association appeared to exist between bacteria and the roots of both grasses with most of the N for the young Aleman pasture being fixed N, whereas the fixed N supply for the older Hymenachne pasture was supplemented by the mineralization of organic N

Denitrification and N2O emission from forested and cultivated alluvial clay soil.

Restored forested wetlands reduce N loads in surface discharge through plant uptake and denitrification. While removal of reactive N reduces impact on receiving waters, it is unclear whether enhanced denitrification also enhances emissions of the greenhouse gas N2O, thus compromising the water-quality benefits of restoration. This study compares denitrification rates and N2O:N2 emission ratios from Sharkey clay soil in a mature bottomland forest to those from an adjacent cultivated site in the Lower Mississippi Alluvial Valley. Potential denitrification of forested soil was 2.4 times of cultivated soil. Using intact soil cores, denitrification rates of forested soil were 5.2, 6.6 and 2.0 times those of cultivated soil at 70, 85 and 100% water-filled pore space (WFPS), respectively. When NO3 was added, N2O emissions from forested soil were 2.2 times those of cultivated soil at 70% WFPS. At 85 and 100% WFPS, N2O emissions were not significantly different despite much greater denitrification rates in the forested soil because N2O:N2 emission ratios declined more rapidly in forested soil as WFPS increased. These findings suggest that restoration of forested wetlands to reduce NO3 in surface discharge will not contribute significantly to the atmospheric burden of N2O

The Phenylpropanoid Pathway in Arabidopsis

The phenylpropanoid pathway serves as a rich source of metabolites in plants, being required for the biosynthesis of lignin, and serving as a starting point for the production of many other important compounds, such as the flavonoids, coumarins, and lignans. In spite of the fact that the phenylpropanoids and their derivatives are sometimes classified as secondary metabolites, their relevance to plant survival has been made clear via the study of Arabidopsis and other plant species. As a model system, Arabidopsis has helped to elucidate many details of the phenylpropanoid pathway, its enzymes and intermediates, and the interconnectedness of the pathway with plant metabolism as a whole. These advances in our understanding have been made possible in large part by the relative ease with which mutations can be generated, identified, and studied in Arabidopsis. Herein, we provide an overview of the research progress that has been made in recent years, emphasizing both the genes (and gene families) associated with the phenylpropanoid pathway in Arabidopsis, and the end products that have contributed to the identification of many mutants deficient in the phenylpropanoid metabolism: the sinapate esters