Plasticity of Mouse Dorsal Root Ganglion Neurons by Innate Immune Activation Is Influenced by Electrophysiological Activity.

The complex relationship between inflammation, its effects on neuronal excitability and the ensuing plasticity of dorsal root ganglion (DRG) sensory neurons remains to be fully explored. In this study, we have employed a system of experiments assessing the impact of inflammatory conditioned media derived from activated immune cells on the excitability and activity of DRG neurons and how this relates to subsequent growth responses of these cells. We show here that an early phase of increased neuronal activity in response to inflammatory conditioned media is critical for the engagement of plastic processes and that neuronal excitability profiles are linked through time to the structural phenotype of individual neurons.

THE FAM53C/DYRK1A axis regulates the G1/S transition of the cell cycle.

A growing number of therapies are being developed to target the cell cycle machinery for the treatment of cancer and other human diseases. Consequently, a greater understanding of the factors regulating cell cycle progression becomes essential to help enhance the response to these new therapies. Here, using data from the Cancer Dependency Map, we identified the poorly-studied factor FAM53C as a new regulator of cell cycle progression.

Landscape-scale drivers of spatial dynamics and genetic diversity in an emerging wildlife pathogen.

Aquatic pathogens often cannot tolerate drying, and thus their spread, and diversity across a landscape may depend on interactions between hydrological conditions and the movement of infected hosts. The aquatic fungus Batrachochytrium dendrobatidis (Bd) is a nearly ubiquitous pathogen of amphibians and particular lineages have been associated with host declines. By coupling amphibian surveys with molecular pathogen detection and genotyping techniques, we characterized the spatial dynamics and genetic diversity of Bd on a landscape containing both permanent and ephemeral ponds.