Streptococcal M1 protein constructs a pathological host fibrinogen network

M1 protein, a major virulence factor of the leading invasive strain of group A Streptococcus, is sufficient to induce toxic-shock-like vascular leakage and tissue injury. These events are triggered by the formation of a complex between M1 and fibrinogen that, unlike M1 or fibrinogen alone, leads to neutrophil activation. Here we provide a structural explanation for the pathological properties of the complex formed between streptococcal M1 and human fibrinogen. A conformationally dynamic coiled-coil dimer of M1 was found to organize four fibrinogen molecules into a specific cross-like pattern. This pattern supported the construction of a supramolecular network that was required for neutrophil activation but was distinct from a fibrin clot. Disruption of this network into other supramolecular assemblies was not tolerated. These results have bearing on the pathophysiology of streptococcal toxic shock.     

Trampling disturbance and recovery of cryptogamic soil crusts in Grand Canyon National Park

Cryptogamic soil crusts in Grand Canyon National Park were trampled by hikers, under controlled conditions, to determine how rapidly they were pulverized and how rapidly they recovered. Only 15 trampling passes were required to destroy the structure of the crusts; visual evidence of bacteria and cryptogam cover was reduced to near zero after 50 passes. Soil crusts redeveloped in just one to three years, and after five years the extensive bacteria and cryptogam cover left little visual evidence of disturbance. Surface irregularity remained low after five years, however, suggesting that recovery was incomplete.     

Microbial spatial heterogeneity in microbiotic crusts in Colorado National Monument. II Bacteria

Microbial spatial heterogeneity and bacterial composition of homogeneous surface soils showing evident microbiotic crust development located under Utah juniper canopies in Colorado National Monument were studied. Four distinct homogeneous sampling sites positioned along a 12-m transect were compared on the basis of bacterial density and taxa composition. Bacterial densities showed a range differing by several orders of magnitude. In comparisons of adjacent soil samples or samples taken from two different sampling sites within close proximity, adjacent samples showed no more similarity to each other on the basis of bacterial density or taxa composition than did more widely separated samples. The bacterial composition of these soils included members of the genera Bacillus , Micrococcus , and Arthrobacter . Actinomycetes were also prevalent.     

Molecular basis for differences between human joints

The molecular program of a cell determines responses including induction or inhibition of genes for function and activity, and this is true of the cells within articular cartilage, a major functional component of the joint. While our studies have previously focussed on differences in the molecular programs of the cells within the superficial and deep zones, we have recently begun to focus on relative differences between joints, such as the knee and ankle. In the human, these joints vary greatly in their susceptibility to joint diseases, such as osteoarthritis (OA). We have predicted that there would be a molecular basis for differences between joints that could lead to differences in susceptibility to OA, if inherent pathways locked into the resident cells induce differences in their response to their environment. We have been able to show that there are differences between the matrix components and water content; these properties correspond to a higher equilibrium modulus and dynamic stiffness but lower hydraulic permeability and serve to make the ankle cartilage stiffer, slowing movement of molecules through the cartilage. In addition to these biochemical differences in the cartilage matrix, we have also identified relative differences in the strength of the response to stimulation of chondrocytes from knee and ankle. The stronger response of the knee chondrocytes includes factors that increase damage to the cartilage matrix, such as a depression of matrix synthesis and increased enzyme activity. This response by the knee chondrocytes results in enzyme damage to the matrix that the cells may not be able to repair, while the weaker response of the ankle chondrocytes may allow the cells to repair their matrix damage.