Nitrogen-tillage-residue management

Summary NCSWAP (nitrogen and carbon cycling in soil, water and plant) is a simulation model of the soil-crop-water system which integrates water flow dynamics, crop growth, N transformations, tillage and residue effects, soil temperature, and solute transport. A small plot field study was initiated in May of 1980 to determine the effects of N rate (2 or 20 g N/m²), tillage (rototill or no-till), and residue management system (residue return or noresidue) on soil parameters, and maize (Zea mays L.) production.Significant differences due to treatments (N rate, tillage, and residue) were not detected in 1981 for the measured soil-plant parameters including soil moisture, yield, and N uptake. Therefore, two representative treatment combinations (N rates of 2 or 20 g N/m²-tilled-no residue) characterized the field research data. Calculated and observed data sets were compared for several parameters including: (1) soluble NO₃–N, (2) N leaching losses (3) plant total-N and¹⁵N, (4) root growth, (5) soil moisture, and (6) fertilizer efficiency.The objectives of this study were to initiate the validation process of the model NCSWAP, and to illustrate how NCSWAP can be used as a research tool to infer operational characteristics of the N cycle.Contribution of the Soil and Water Management Research Unit, USDA-ARS, and the Department of Soil Science, University of Minnesota, St. Paul, MN 55108. Minn Agric. Exp. Sta., Sci. J., Ser. Paper 13907.Senior Laboratory Technician; Research Chemist, USDA-ARS and Professor; Professor of Soil Microbiology; and Soil Scientist, USDA-ARS and Assistant Professor; all Department of Soil Science, University of Minnesota, respectively. Inquiries about NCSWAP should be sent to J. A. E. Molina.     

Regulation of one type of Ca2+ current in smooth muscle cells by diacylglycerol and acetylcholine

Electrophysiological recordings from freshly dissociated smooth muscle cells from the stomach of the toad Bufo marinus revealed two types of Ca2+ currents. One has a low threshold of activation and inactivates rapidly; the other has a high threshold of activation and inactivates more slowly. Acetylcholine (ACh) increased the high-threshold current but not the low-threshold current. The synthetic diacylglycerol analog sn-1,2-dioctanoylglycerol, an activator of protein kinase C (PKC), mimicked these effects of ACh on Ca2+ currents. However, another diacylglycerol analog, 1,2-dioctanoyl-3-thioglycerol, which has a closely related structure but does not activate PKC, failed to increase the Ca2+ current. The same was true of 1,2-dioctanoyl-3-chloropropanediol, an analog that even at high concentrations only minimally activates PKC. These results suggest that diacylglycerol may be the second messenger mediating the effects of ACh on one type of voltage-activated Ca2+ channel, possibly by activating PKC.     

Fanconi anemia D2 protein is an apoptotic target mediated by caspases

FANCD2, a key factor in the FANC-BRCA1 pathway is monoubiquitinated and targeted to discrete nuclear foci following DNA damage. Since monoubiquitination of FANCD2 is a crucial indicator for cellular response to DNA damage, we monitored the fate of FANCD2 and its monoubiquitination following DNA damage. Disappearance of FANCD2 protein was induced following DNA damage in a dose-dependent manner, which correlated with degradation of BRCA1 and poly-ADP ribose polymerase (PARP), known targets for caspase-mediated apoptosis. Disappearance of FANCD2 was not affected by a proteasome inhibitor but was blocked by a caspase inhibitor. DNA damage-induced disappearance of FANCD2 was also observed in cells lacking FANCA, suggesting that disappearance of FANCD2 does not depend on FANC-BRCA1 pathway and FANCD2 monoubiquitination. In keeping with this, cells treated with TNF-α, an apoptotic stimulus without causing any DNA damage, also induced disappearance of FANCD2 without monoubiquitination. Together, our data suggest that FANCD2 is a target for caspase-mediated apoptotic pathway, which may be an early indicator for apoptotic cell death.