Recent investigations of the 0-5 geomagnetic field recorded by lava flows

Sherpa Romeo green journal (pre or post print only)We present a synthesis of paleomagnetic directional data collected from 873 lava flows at 17 different locations under the collaborative Time Averaged geomagnetic Field Initiative (TAFI). The data range from 05 Ma in age, and provide new high quality data with improved spatial coverage. Data quality at each site is measured using k, the best estimate of the Fisherian precision parameter, and its influence on inclination anomaly and VGP dispersion is evaluated by systematically excluding data with successively higher values of k. When combined with regional compilations from NW USA, SW USA, Japan, New Zealand, Hawaii, Mexico, S. Pacific and the Indian Ocean, a data set of 2283 pairs of declination and inclination data, with k>100, and VGP latitudes greater than 45 is obtained. This is a more than 7fold increase over similar quality data in the existing Global Paleomagnetic Database (GPMDB). The new data set spans 78 S to 53 N, and has sufficient temporal and spatial sampling to allow characterization of latitudinal variations in the timeaveraged field (TAF) and paleosecular variation (PSV) for the Brunhes and Matuyama epochs, and for the 0–5 Myr interval combined. PSV, as measured by dispersion of virtual geomagnetic poles, shows less latitudinal variation than predicted by current statistical PSV models. Variation of inclination anomaly with latitude is assessed using 2parameter zonal TAF models – these have axial quadrupole contributions of 2% – 4% of the axial dipole term, and axial octupole contributions of 3% – 5%. Approximately 2% of the octupole signature is likely the result of bias incurred by averaging unit vectors. The new data set provides significant improvement over previous compilations, and can contribute to a new generation of global paleomagnetic field models.Ye

Genetic Dissection of an Exogenously Induced Biofilm in Laboratory and Clinical Isolates of E. coli

Microbial biofilms are a dominant feature of many human infections. However, developing effective strategies for controlling biofilms requires an understanding of the underlying biology well beyond what currently exists. Using a novel strategy, we have induced formation of a robust biofilm in Escherichia coli by utilizing an exogenous source of poly-N-acetylglucosamine (PNAG) polymer, a major virulence factor of many pathogens. Through microarray profiling of competitive selections, carried out in both transposon insertion and over-expression libraries, we have revealed the genetic basis of PNAG-based biofilm formation. Our observations reveal the dominance of electrostatic interactions between PNAG and surface structures such as lipopolysaccharides. We show that regulatory modulation of these surface structures has significant impact on biofilm formation behavior of the cell. Furthermore, the majority of clinical isolates which produced PNAG also showed the capacity to respond to the exogenously produced version of the polymer

Staphylococcus aureus RNAIII Binds to Two Distant Regions of coa mRNA to Arrest Translation and Promote mRNA Degradation

Staphylococcus aureus RNAIII is the intracellular effector of the quorum sensing system that temporally controls a large number of virulence factors including exoproteins and cell-wall-associated proteins. Staphylocoagulase is one major virulence factor, which promotes clotting of human plasma. Like the major cell surface protein A, the expression of staphylocoagulase is strongly repressed by the quorum sensing system at the post-exponential growth phase. Here we used a combination of approaches in vivo and in vitro to analyze the mechanism used by RNAIII to regulate the expression of staphylocoagulase. Our data show that RNAIII represses the synthesis of the protein through a direct binding with the mRNA. Structure mapping shows that two distant regions of RNAIII interact with coa mRNA and that the mRNA harbors a conserved signature as found in other RNAIII-target mRNAs. The resulting complex is composed of an imperfect duplex masking the Shine-Dalgarno sequence of coa mRNA and of a loop-loop interaction occurring downstream in the coding region. The imperfect duplex is sufficient to prevent the formation of the ribosomal initiation complex and to repress the expression of a reporter gene in vivo. In addition, the double-strand-specific endoribonuclease III cleaves the two regions of the mRNA bound to RNAIII that may contribute to the degradation of the repressed mRNA. This study validates another direct target of RNAIII that plays a role in virulence. It also illustrates the diversity of RNAIII-mRNA topologies and how these multiple RNAIII-mRNA interactions would mediate virulence regulation