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