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Winter mortality can strongly affect the population dynamics of blue crabs (Callinectes sapidus) near poleward range limits. We simulated winter in the lab to test the effects of temperature, salinity, and estuary of origin on blue crab winter mortality over three years using a broad range of crab sizes from both Great South Bay and Chesapeake Bay. We fit accelerated failure time models to our data and to data from prior blue crab winter mortality experiments, illustrating that, in a widely distributed, commercially valuable marine decapod, temperature, salinity, size, estuary of origin, and winter duration were important predictors of winter mortality. Furthermore, our results suggest that extrapolation of a Chesapeake Bay based survivorship model to crabs from New York estuaries yielded poor fits. As such, the severity and duration of winter can impact northern blue crab populations differently along latitudinal gradients. In the context of climate change, future warming could possibility confer a benefit to crab populations near the range edge that are currently limited by temperature-induced winter mortality by shifting their range edge poleward, but care must be taken in generalizing from models that are developed based on populations from one part of the range to populations near the edges, especially for species that occupy large geographical areas. [ABSTRACT FROM AUTHOR]

In humans, congenital and hereditary skin diseases associated with epidermal cell-cell separation (acantholysis) are very rare, and spontaneous animal models of these diseases are exceptional. Our objectives are to report a novel congenital acantholytic dermatosis that developed in Chesapeake Bay retriever dogs. Nine affected puppies in four different litters were born to eight closely related clinically normal dogs. The disease transmission was consistent with an autosomal recessive mode of inheritance. Clinical signs occurred immediately after birth with superficial epidermal layers sloughing upon pressure. At three month of age, dogs exhibited recurrent superficial skin sloughing and erosions at areas of friction and mucocutaneous junctions; their coat was also finer than normal and there were patches of partial hair loss. At birth, histopathology revealed severe suprabasal acantholysis, which became less severe with ageing. Electron microscopy demonstrated a reduced number of partially formed desmosomes with detached and aggregated keratin intermediate filaments. Immunostaining for desmosomal adhesion molecules revealed a complete lack of staining for plakophilin-1 and anomalies in the distribution of desmoplakin and keratins 10 and 14. Sequencing revealed a homozygous splice donor site mutation within the first intron of PKP1 resulting in a premature stop codon, thereby explaining the inability to detect plakophilin-1 in the skin. Altogether, the clinical and pathological findings, along with the PKP1 mutation, were consistent with the diagnosis of ectodermal dysplasia-skin fragility syndrome with plakophilin-1 deficiency. This is the first occurrence of ectodermal dysplasia-skin fragility syndrome in an animal species. Controlled mating of carrier dogs would yield puppies that could, in theory, be tested for gene therapy of this rare but severe skin disease of children. [ABSTRACT FROM AUTHOR]