Climate change effects on plant disease: genomes to ecosystems.

Citation: Garrett, K., . . . & Travers, S. (2006). Climate Change Effects on Plant Disease: Genomes to Ecosystems. Annual Review of Phytopathology, 44(1), 489-509. https://doi.org/10.1146/annurev.phyto.44.070505.143420Research in the effects of climate change on plant disease continues to be limited, but some striking progress has been made. At the genomic level, advances in technologies for the high-throughput analysis of gene expression have made it possible to begin discriminating responses to different biotic and abiotic stressors and potential trade-offs in responses. At the scale of the individual plant, enough experiments have been performed to begin synthesizing the effects of climate variables on infection rates, though pathosystemspecific characteristics make synthesis challenging. Models of plant disease have now been developed to incorporate more sophisticated climate predictions. At the population level, the adaptive potential of plant and pathogen populations may prove to be one of the most important predictors of the magnitude of climate change effects. Ecosystem ecologists are now addressing the role of plant disease in ecosystem processes and the challenge of scaling up from individual infection probabilities to epidemics and broader impacts

Proresolving mediators counter inflammation in stromal cells from patients with Achilles tendon disease

General models of network navigation must contain a deterministic or drift component, encouraging the agent to follow routes of least cost, as well as a random or diffusive component, enabling free wandering. This paper proposes a thermodynamic formalism involving two path functionals, namely an energy functional governing the drift and an entropy functional governing the diffusion. A freely adjustable parameter, the temperature, arbitrates between the conflicting objectives of minimising travel costs and maximising spatial exploration. The theory is illustrated on various graphs and various temperatures. The resulting optimal paths, together with presumably new associated edges and nodes centrality indices, are analytically and numerically investigated

Regulation of toxin and bacteriocin gene expression in Clostridium by interchangeable RNA polymerase sigma factors

International audienceThe production of major extracellular toxins by pathogenic strains of Clostridium botulinum, Clostridium tetani and Clostridium difficile, and a bacteriocin by Clostridium perfringens is dependent on a related group of RNA polymerase sigma-factors. These sigma-factors (BotR, TetR, TcdR and UviA) were shown to be sufficiently similar that they could substitute for one another in in vitro DNA binding and run-off transcription experiments. In cells, however, the sigma-factors fell into two subclasses. BotR and TetR were able to direct transcription of their target genes in a fully reciprocal manner. Similarly, UviA and TcdR were fully interchangeable. Neither BotR nor TetR could substitute for UviA or TcdR, however, and neither UviA nor TcdR could direct transcription of the natural targets of BotR or TetR. The extent of functional interchangeability of the sigma-factors was attributed to the strong conservation of their subregion 4.2 sequences and the conserved -35 sequences of their target promoters, while restrictions on interchangeability were attributed to variations in their subregion 2.4 sequences and the target site -10 sequences. The four sigma-factors have been assigned to group 5 of the sigma(70) family and seem to have arisen from a common ancestral protein that may have co-evolved with the genes whose transcription they direct. A fifth Clostridiumsigma-factor, sigma(Y) of Clostridium acetobutylicum, resembles the TcdR family, but was not functionally interchangeable with members of this family