Prey size and species preferences in the invasive blue crab, Callinectes sapidus: Potential effects in marine and freshwater ecosystems

The blue crab, Callinectes sapidus is an invasive species in the Mediterranean region. In Ebro Delta bays, it poses an important risk for the cultivation of Mediterranean mussel (Mytillus galloprovincialis) and Pacific oyster (Crassostrea gigas). Besides, the species thrives in the Ebro River hosting abundant populations of apple snail (Pomacea maculata) and Asian clam (Corbicula fluminea). Food-preference experiments were conducted to assess the effect of predator and prey sizes and prey type (M. galloprovincialis vs. C. gigas and P. maculata vs. C. fluminea) in predation patterns and its possible causes. Our results show that except for the Pacific oyster, which attains protection at sizes of 50–70 mm and was little consumed (0–16%), the other preys are readily predated, at variable rates (mussels: 38–96%; apple snail: 58–93%, and Asian clam: 67–100%), depending on predator and prey sizes. Juveniles and young blue crab adults showed greater consumption of small and medium mussels and a similar trend occurred with Asian clam. In contrast, large and medium apple snails were more heavily predated by adult blue crabs. Species comparisons also showed higher predation of mussels than oysters (71 vs. 8%), and of apple snail than Asian clam (99 vs. 72%). Once the shell barrier was removed, preference for mussels was still preserved, suggesting a nutritional preference. Our results point the need of fishing blue crab in marine areas to prevent losses in mussel production and highlight the potential control exerted over undesired invasive mollusk species.info:eu-repo/semantics/acceptedVersio

X chromosome inactivation does not necessarily determine the severity of the phenotype in Rett syndrome patients

Rett syndrome (RTT) is a severe neurological disorder usually caused by mutations in the MECP2 gene. Since the MECP2 gene is located on the X chromosome, X chromosome inactivation (XCI) could play a role in the wide range of phenotypic variation of RTT patients; however, classical methylation-based protocols to evaluate XCI could not determine whether the preferentially inactivated X chromosome carried the mutant or the wild-type allele. Therefore, we developed an allele-specific methylation-based assay to evaluate methylation at the loci of several recurrent MECP2 mutations. We analyzed the XCI patterns in the blood of 174 RTT patients, but we did not find a clear correlation between XCI and the clinical presentation. We also compared XCI in blood and brain cortex samples of two patients and found differences between XCI patterns in these tissues. However, RTT mainly being a neurological disease complicates the establishment of a correlation between the XCI in blood and the clinical presentation of the patients. Furthermore, we analyzed MECP2 transcript levels and found differences from the expected levels according to XCI. Many factors other than XCI could affect the RTT phenotype, which in combination could influence the clinical presentation of RTT patients to a greater extent than slight variations in the XCI pattern