Quantifying Pedogenic Carbon Content Within the Boise River Terraces Using Pressurized Calcimetry

Soil carbon is the third largest carbon pool within the global carbon cycle; however, soil carbon amounts are not well quantified, and exchange rates of soil carbon are not well understood. Soil carbon can be divided into organic carbon and inorganic carbon, where inorganic carbon (pedogenic carbonate) is precipitated during soil formation and accumulates over time in semi-arid and arid environments. Calcic soils within the semiarid regions of the Boise Valley result from active pedogenic accumulation of secondary CaCO3 resulting in prominent \u27caliche\u27 layers in soils formed on many of the Boise River terraces. The larger goals of this project are to quantify inorganic carbon sequestered within the Boise River terraces, and investigate rates of carbonate dissolution due to irrigation. This portion of the project focuses on developing methods for measuring inorganic carbon content in soils using pressurized calcimetry. Samples are acidified within a closed system to form CO2 under constant temperature, allowing time-pressure readings to delineate the levels of inorganic carbon present. Future work will reveal trends in carbon content with depth in individual soil profiles, and variations in carbon content for terraces of different ages

Escherichia Coli RecG Functionally Suppresses Human Bloom Syndrome Phenotypes

Defects in the human BLM gene cause Bloom syndrome, notable for early development of tumors in a broad variety of tissues. On the basis of sequence similarity, BLM has been identified as one of the five human homologs of RecQ from Escherichia coli. Nevertheless, biochemical characterization of the BLM protein indicates far greater functional similarity to the E. coli RecG protein and there is no known RecG homolog in human cells. To explore the possibility that the shared biochemistries of BLM and RecG may represent an example of convergent evolution of cellular function where in humans BLM has evolved to fulfill the genomic stabilization role of RecG, we determined whether expression of RecG in human BLM-deficient cells could suppress established functional cellular Bloom syndrome phenotypes. We found that RecG can indeed largely suppress both the definitive elevated sister chromatid exchange phenotype and the more recently demonstrated gene cluster instability phenotype of BLM-deficient cells. In contrast, expression of RecG has no impact on either of these phenotypes in human cells with functional BLM protein. These results suggest that the combination of biochemical activities shared by RecG and BLM fill the same evolutionary niche in preserving genomic integrity without requiring exactly identical molecular mechanisms