Cross-scale drivers of plant trait distributions in a fragmented forest landscape

During community assembly, plant functional traits are under selective pressure from processes operating at multiple spatial scales. However, in fragmented landscapes, there is little understanding of the relative importance of local-, patch- and landscape-scale processes in shaping trait distributions. Here, we investigate cross-scale influences of landscape change on traits that dictate plant life history strategies in re-assembling plant communities in a fragmented landscape in eastern China. Using forest dynamics plots (FDPs) on 29 land-bridge islands in which all woody plants have been georeferenced and identified to species, we characterized and derived two composite measures of trait variation, representing variation across the leaf economics spectrum and plant size. We then tested for trait shifts in response to local-, patch- and landscape-scale factors, and their potential cross-scale interactions. We found substantial community-wide trait changes along local-scale gradients (i.e. forest edge to interior): more acquisitive leaf economic traits and larger sized species occurred at edges, with a significant increase in trait means and trait range. Moreover, there were significant cross-scale interaction effects of patch and landscape variables on local-scale edge effects. Altered spatial arrangement of habitat in the surrounding landscape (i.e. declining habitat amount and increasing patch density), as well as decreasing area at the patch level, exacerbated edge effects on traits distributions. We suggest that synergistic interactions of landscape- and patch-scale processes, such as dispersal limitation, on local-scale environmental filtering at edges, together shape the spatial distributions of plant life history strategies in fragmented plant communities.     

Ferroptosis is involved in alcohol-induced cell death in vivo and in vitro

ABSTRACT

A critical pathogenic factor in the development of lethal liver failure is cell death induced by the accumulation of lipid reactive oxygen species. In this study, we discovered and illuminated a new mechanism that led to alcoholic liver disease via ferroptosis, an iron-dependent regulated cell death. Study in vitro showed that both necroptosis inhibitor and ferroptosis inhibitors performed significantly protective effect on alcohol-induced cell death, while apoptosis inhibitor and autophagy inhibitor had no such effect. Our data also indicated that alcohol caused the accumulation of lipid peroxides and the mRNA expression of prostaglandin-endoperoxide synthase 2, reduced the protein expression of the specific light-chain subunit of the cystine/glutamate antiporter and glutathione peroxidase 4. Importantly, ferrostatin-1 significantly ameliorated liver injury that was induced by overdosed alcohol both in vitro and in vivo. These findings highlight that targeting ferroptosis serves as a hepatoprotective strategy for alcoholic liver disease treatment.     

Novel (p)ppGpp0 suppressor mutations reveal an unexpected link between methionine catabolism and GTP synthesis in Bacillus subtilis

In bacteria, guanosine (penta)tetra-phosphate ([p]ppGpp) is essential for controlling intracellular metabolism that is needed to adapt to environmental changes, such as amino acid starvation. The (p)ppGpp⁰ strain of Bacillus subtilis, which lacks (p)ppGpp synthetase, is unable to form colonies on minimal medium. Here, we found suppressor mutations in the (p)ppGpp⁰ strain, in the purine nucleotide biosynthesis genes, prs, purF and rpoB/C, which encode RNA polymerase core enzymes. In comparing our work with prior studies of ppGpp⁰ suppressors, we discovered that methionine addition masks the suppression on minimal medium, especially of rpoB/C mutations. Furthermore, methionine addition increases intracellular GTP in rpoB suppressor and this effect is decreased by inhibiting GTP biosynthesis, indicating that methionine addition activated GTP biosynthesis and inhibited growth under amino acid starvation conditions in (p)ppGpp⁰ backgrounds. Furthermore, we propose that the increase in intracellular GTP levels induced by methionine is due to methionine derivatives that increase the activity of the de novo GTP biosynthesis enzyme, GuaB. Our study sheds light on the potential relationship between GTP homeostasis and methionine metabolism, which may be the key to adapting to environmental changes.