No evidence for a dilution effect of the non-native snail, Potamopyrgus antipodarum, on native snails.

The dilution effect can occur by a range of mechanisms and results in reduced parasite prevalence in host taxa. In invaded ecosystems, the dilution effect can benefit native species if non-native species, acting as resistant or less competent hosts, reduce rates of parasitic infections in native species. In field experiments, we assessed whether manipulating biomass of the non-native snail, Potamopyrgus antipodarum, caused a dilution effect by reducing trematode infections in three taxa of native snails. In contrast to many studies showing resistant or less competent non-native hosts can "dilute" or reduce infection rates, we found no evidence for a dilution effect reducing infection rates of any of the native snails. We suggest that a dilution effect may not have occurred because most trematode taxa are highly host specific, and thus the trematode transmission stages did not recognize the invasive snail as a possible host. In this case, community composition appears to be important in influencing the dilution effect

Mitochondrial citrate metabolism and efflux regulate BeWo differentiation

Abstract Cytotrophoblasts fuse to form and renew syncytiotrophoblasts necessary to maintain placental health throughout gestation. During cytotrophoblast to syncytiotrophoblast differentiation, cells undergo regulated metabolic and transcriptional reprogramming. Mitochondria play a critical role in differentiation events in cellular systems, thus we hypothesized that mitochondrial metabolism played a central role in trophoblast differentiation. In this work, we employed static and stable isotope tracing untargeted metabolomics methods along with gene expression and histone acetylation studies in an established BeWo cell culture model of trophoblast differentiation. Differentiation was associated with increased abundance of the TCA cycle intermediates citrate and α-ketoglutarate. Citrate was preferentially exported from mitochondria in the undifferentiated state but was retained to a larger extent within mitochondria upon differentiation. Correspondingly, differentiation was associated with decreased expression of the mitochondrial citrate transporter (CIC). CRISPR/Cas9 disruption of the mitochondrial citrate carrier showed that CIC is required for biochemical differentiation of trophoblasts. Loss of CIC resulted in broad alterations in gene expression and histone acetylation. These gene expression changes were partially rescued through acetate supplementation. Taken together, these results highlight a central role for mitochondrial citrate metabolism in orchestrating histone acetylation and gene expression during trophoblast differentiation