Spatial Prediction of Soil Organic Matter Content Using Cokriging with Remotely Sensed Data

Accurately measuring soil organic matter content (SOM) in paddy fields is important because SOM is one of the key soil properties controlling nutrient budgets in agricultural production systems. Estimation of this soil property at an acceptable level of accuracy is important; especially in the case when SOM exhibits strong spatial dependence and its measurement is a time- and labor-consuming procedure. This study was conducted to evaluate and compare spatial estimation by kriging and cokriging with remotely sensed data to predict SOM using limited available data for a 367-km(2) study area in Haining City, Zhejiang Province, China. Measured SOM ranged from 5.7 to 40.4 g kg(-1), with a mean of 19.5 g kg(-1). Correlation analysis between the SOM content of 131 soil samples and the corresponding digital number (DN) of six bands (Band 1-5 and Band 7) of Landsat Enhanced Thematic Mapper (ETM) imagery showed that correlation between SOM and DN of Band 1 was the highest (r= -0.587). We used the DN of Band I as auxiliary data for the SOM prediction, and used descriptive statistics and the kriging standard deviation (STD) to compare the reliabilities of the predictions. We also used cross-validation to validate the SOM prediction. Results indicate that cokriging with remotely sensed data was superior to kriging in the case of limited available data and the moderately strong linear relationship between remotely sensed data and SOM content. Remotely sensed data such as Landsat ETM imagery have the potential as useful auxiliary variables for improving the precision and reliability of SOM prediction

Complement Component C1q Programs a Pro-Efferocytic Phenotype while Limiting TNFα Production in Primary Mouse and Human Macrophages

Deficiency in complement component C1q is associated with an inability to clear apoptotic cells (efferocytosis) and aberrant inflammation in lupus, and identification of the pathways involved in these processes should reveal important regulatory mechanisms in lupus and other autoimmune or inflammatory diseases. In this study, C1q-dependent regulation of TNFα/IL-6 expression and efferocytosis was investigated using primary mouse bone marrow-derived macrophages and human monocyte-derived macrophages. C1q downregulated LPS-dependent TNFα production in mouse and human macrophages. While prolonged stimulation with C1q (18 h) was required to elicit a dampening of TNFα production from mouse macrophages, the human macrophages responded to C1q with immediate downregulation of TNFα. IL-6 production was unchanged in mouse and upregulated by human macrophages following prolonged stimulation with C1q. Our previous studies indicated that C1q programmed enhanced efferocytosis in mouse macrophages by enhancing expression of Mer tyrosine kinase and its ligand Gas6, a receptor–ligand pair that also inhibits proinflammatory signaling. Here, we demonstrated that C1q-dependent programming of human macrophage efferocytosis required protein synthesis; however, neither Mer nor the related receptor Axl was upregulated in human cells. In addition, while the C1q-collagen-like tails are sufficient for promoting C1q-dependent phagocytosis of antibody-coated targets, the C1q-tails failed to program enhanced efferocytosis or dampen TNFα production. These data further elucidate the mechanisms by which C1q regulates proinflammatory signaling and efferocytosis in macrophages, functions that are likely to influence the progression of autoimmunity and chronic inflammation

Mouse ES cell–derived cardiac precursor cells are multipotent and facilitate identification of novel cardiac genes

Although the differentiation of ES cells to cardiomyocytes has been firmly established, the extent to which corresponding cardiac precursor cells can contribute to other cardiac populations remains unclear. To determine the molecular and cellular characteristics of cardiac-fated populations derived from mouse ES (mES) cells, we isolated cardiac progenitor cells (CPCs) from differentiating mES cell cultures by using a reporter cell line that expresses GFP under the control of a cardiac-specific enhancer element of Nkx2-5, a transcription factor expressed early in cardiac development. This ES cell–derived CPC population initially expressed genetic markers of both stem cells and mesoderm, while differentiated CPCs displayed markers of 3 distinct cell lineages (cardiomyocytes, vascular smooth muscle cells, and endothelial cells) — Flk1 (also known as Kdr), c-Kit, and Nkx2-5, but not Brachyury — and subsequently expressed Isl1. Clonally derived CPCs also demonstrated this multipotent phenotype. By transcription profiling of CPCs, we found that mES cell–derived CPCs displayed a transcriptional signature that paralleled in vivo cardiac development. Additionally, these studies suggested the involvement of genes that we believe were previously unknown to play a role in cardiac development. Taken together, our data demonstrate that ES cell–derived CPCs comprise a multipotent precursor population capable of populating multiple cardiac lineages and suggest that ES cell differentiation is a valid model for studying development of multiple cardiac-fated tissues

S-Phase Checkpoint Genes Safeguard High-Fidelity Sister Chromatid Cohesion

Cohesion establishment and maintenance are carried out by proteins that modify the activity of Cohesin, an essential complex that holds sister chromatids together. Constituents of the replication fork, such as the DNA polymerase α-binding protein Ctf4, contribute to cohesion in ways that are poorly understood. To identify additional cohesion components, we analyzed a ctf4Δ synthetic lethal screen performed on microarrays. We focused on a subset of ctf4Δ-interacting genes with genetic instability of their own. Our analyses revealed that 17 previously studied genes are also necessary for the maintenance of robust association of sisters in metaphase. Among these were subunits of the MRX complex, which forms a molecular structure similar to Cohesin. Further investigation indicated that the MRX complex did not contribute to metaphase cohesion independent of Cohesin, although an additional role may be contributed by XRS2. In general, results from the screen indicated a sister chromatid cohesion role for a specific subset of genes that function in DNA replication and repair. This subset is particularly enriched for genes that support the S-phase checkpoint. We suggest that these genes promote and protect a chromatin environment conducive to robust cohesion