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Karachaliou, E.

Publications and source records attributed to Karachaliou, E..

2 recordsLinked to original sources

Urbanization is associated with reduced genetic diversity in marine fish populations

The economic and ecological benefits of living by the ocean have led many coastal settlements to grow into large densely populated cities. Large coastal cities have had considerable environmental effects on marine ecosystems through resource extraction, waste disposal, and use for transportation. Thus, it is important to understand the consequences of urbanization and human activities on evolutionary processes and biodiversity in marine fishes. Using published population genetic datasets for marine fishes amounting to 75,496 individuals sampled from 73 species at 1143 sample sites throughout the worlds oceans, we evaluated how human population density and a composite measure of cumulative human impacts affected genetic diversity and differentiation. We found that genetic diversity was significantly lower in marine fish populations associated with denser human populations regardless of species and locality. The effects of cumulative human impacts on genetic diversity were less prominent, perhaps due to this measure capturing more spatially varying processes. Urbanization in coastal regions has degraded marine biodiversity in a way that erodes adaptive potential for marine fish populations. This highlights the need to mitigate threats from human activities and focus efforts on sustainable urban planning and resource use to conserve marine biodiversity sustaining coastal fisheries and ecosystems.

evolutionary biology↗

Common synaptic phenotypes arising from diverse mutations in the human NMDA receptor subunit GluN2A

Dominant mutations in the human gene GRIN2A, encoding NMDA receptor (NMDAR) subunit GluN2A, make a significant and growing contribution to the catalogue of published single-gene epilepsies. Understanding the disease mechanism in these epilepsy patients is complicated by the surprising diversity of effects that the mutations have on NMDARs. We have examined the cell-autonomous effect of five GluN2A mutations, 3 loss-of-function and 2 gain-of-function, on evoked NMDAR-mediated synaptic currents (NMDA-EPSCs) in CA1 pyramidal neurons in cultured hippocampal slices. Despite the mutants differing in their functional incorporation at synapses, prolonged NMDA-EPSC current decays (with only marginal changes in charge transfer) were a common effect for both gain- and loss-of-function mutants. Modelling NMDA-EPSCs with mutant properties in a CA1 neuron revealed that the effect of GRIN2A mutations can lead to abnormal temporal integration and spine calcium dynamics during trains of concerted synaptic activity. Investigations beyond establishing the molecular defects of GluN2A mutants are much needed to understand their impact on synaptic transmission.

neuroscience↗