The intD mobile genetic element from Dichelobacter nodosus, the causative agent of ovine footrot, is associated with the benign phenotype.

The Gram-negative anaerobic pathogen Dichelobacter nodosus is the principal causative agent of footrot in sheep. The intA, intB and intC elements are mobile genetic elements which integrate into two tRNA genes downstream from csrA (formerly glpA) and pnpA in the D. nodosus chromosome. CsrA homologues act as global repressors of virulence in several bacterial pathogens, as does polynucleotide phosphorylase, the product of pnpA. We have proposed a model in which virulence in D. nodosus is controlled in part by the integration of genetic elements downstream from csrA and pnpA, altering the expression of these putative global regulators of virulence. We describe here a novel integrated genetic element, the intD element, which is 32kb in size and contains an integrase gene, intD, several genes related to genes on other integrated elements of D. nodosus, a type IV secretion system and a putative mobilisation region, suggesting that the intD element has a role in the transfer of other genetic elements. Most of the D. nodosus strains examined which contained the intD gene were benign, with intD integrated next to pnpA, supporting our previous observation that virulent strains of D. nodosus have the intA element next to pnpA.

A physics-based earthquake simulator replicates seismic hazard statistics across California.

Seismic hazard models are important for society, feeding into building codes and hazard mitigation efforts. These models, however, rest on many uncertain assumptions and are difficult to test observationally because of the long recurrence times of large earthquakes. Physics-based earthquake simulators offer a potentially helpful tool, but they face a vast range of fundamental scientific uncertainties. We compare a physics-based earthquake simulator against the latest seismic hazard model for California. Using only uniform parameters in the simulator, we find strikingly good agreement of the long-term shaking hazard compared with the California model. This ability to replicate statistically based seismic hazard estimates by a physics-based model cross-validates standard methods and provides a new alternative approach needing fewer inputs and assumptions for estimating hazard.

Transition regimes for growing crack populations.

Numerous observational papers on crack populations in the material and geological sciences suggest that cracks evolve in such a way as to organize in specific patterns. However, very little is known about how and why the self-organization comes about. We use a model of tensile-like cracks with friction in order to study the time and space evolution of normal faults. The premise of this spring-block analog is that one could model crustal deformation for long time scales assuming a brittle layer coupled to a ductile substrate. The long time-scale physics incorporated into the model are slip-weakening friction, strain-hardening rheology for coupling the two layers, and randomly distributed yield strength of the brittle layer. We investigate how the evolution of populations of cracks depends on these three effects, using linear stability analysis to calculate the stable regimes for the friction as well as numerical simulations to model the nonlinear interactions of the cracks. We find that we can scale the problem to reduce the relevant parameters to a single one, the slip weakening. We show that the distribution of lengths of active cracks makes a transition from an exponential at very low strains, where crack nucleation prevails, to a power law at low to intermediate strains, where crack growth prevails, to an exponential distribution of the largest cracks at higher strains, where coalescence dominates. There is evidence of these different length distributions in continental and oceanic normal faults. For continental deformation the strain is low, and the faults have power-law frequency-size distributions. For mid-ocean ridge flanks the strain is greater, up to an order of magnitude higher than the continental strain, and faults have exponential-like frequency-size distributions. No theory has been offered to explain this difference in the distributions of continental and mid-ocean faults. In this paper we argue that they are indicative of different stages of evolution. The former faults are at an early stage of relatively small deformation, while the latter are at a later stage of the evolution. For high strain the faults reach a saturation regime with system size cracks evenly spaced in proportion to the brittle layer thickness. We asymptotically approximate the time space evolution of faults as a long time-scale phenomenon, thereby avoiding modeling the short time-scale earthquakes. We show that this assumption is valid, which implies that the faults that creep and faults with earthquakes display the same time and space evolutions.

Isolation of the Bacteriophage DinoHI from Dichelobacter nodosus and its Interactions with other Integrated Genetic Elements.

The Gram-negative anaerobic pathogen Dichelobacter nodosus carries several genetic elements that integrate into the chromosome. These include the intA, intB, intC and intD elements, which integrate adjacent to csrA and pnpA, two putative global regulators of virulence and the virulence-related locus, vrl, which integrates into ssrA. Treatment of D. nodosus strains with ultraviolet light resulted in the isolation of DinoHI, a member of the Siphoviridae and the first bacteriophage to be identified in D. nodosus. Part of the DinoHI genome containing the packaging site is found in all D. nodosus strains tested and is located at the end of the vrl, suggesting a role for DinoHI in the transfer of the vrl by transduction. Like the intB element, the DinoHI genome contains a copy of regA which has similarity to the repressors of lambdoid bacteriophages, suggesting that the maintenance of DinoHI and the intB element may be co-ordinately controlled.