Biological activity exceeds biogenic structure in influencing sediment nitrogen cycling in experimental oyster reefs

Oysters are estuarine ecosystem engineers, in that their physical structure and biological function affect ecosystem processes such as organic matter and nutrient cycling. Oysters deliver material to the sediments through biodeposition and sedimentation caused by modification of flow around the reef. We conducted an experiment to distinguish between biotic effects and physical structure of oyster reefs on sediment nitrogen cycling. Experimental reefs consisting of live oysters, oyster shells alone and mudflats (controls) were sampled for a period of 4 wk for sediment organic matter, C and N content and fluxes of nitrogen (NH4 +, NOX and N2) and oxygen (O2). We hypothesized that the biological activity of the oyster would deposit more, higher quality organic matter compared to deposition from flow modification alone, thus facilitating denitrification and having a larger impact on sediment nitrogen cycling. Compared to the controls, the live oyster experimental reefs increased sediment denitrification by 61% and the shell experimental reefs showed a 24% increase. The live oyster experimental reef also had the largest O2 demand and NH4 + production. Reef structure likely increased organic matter deposition, but the higher quality and larger quantity of organic matter associated with live oysters increased denitrification and microbial respiration. This experiment shows that the ecosystem service of nitrogen removal provided by oysters is primarily driven by the biological function of the oysters and secondarily from the physical structure of the reef. Our increased understanding of how oysters engineer ecosystems and modify nutrient cycling can help guide future oyster restoration effort

Parallelized Manipulation of Adherent Living Cells by Magnetic Nanoparticles-Mediated Forces

The remote actuation of cellular processes such as migration or neuronal outgrowth is a challenge for future therapeutic applications in regenerative medicine. Among the different methods that have been proposed, the use of magnetic nanoparticles appears to be promising, since magnetic fields can act at a distance without interactions with the surrounding biological system. To control biological processes at a subcellular spatial resolution, magnetic nanoparticles can be used either to induce biochemical reactions locally or to apply forces on different elements of the cell. Here, we show that cell migration and neurite outgrowth can be directed by the forces produced by a switchable parallelized array of micro-magnetic pillars, following the passive uptake of nanoparticles. Using live cell imaging, we first demonstrate that adherent cell migration can be biased toward magnetic pillars and that cells can be reversibly trapped onto these pillars. Second, using differentiated neuronal cells we were able to induce events of neurite outgrowth in the direction of the pillars without impending cell viability. Our results show that the range of forces applied needs to be adapted precisely to the cellular process under consideration. We propose that cellular actuation is the result of the force on the plasma membrane caused by magnetically filled endo-compartments, which exert a pulling force on the cell periphery

Mechanism of homodimeric cytokine receptor activation and dysregulation by oncogenic mutations

Homodimeric class I cytokine receptors are assumed to exist as preformed dimers that are activated by ligand-induced conformational changes. We quantified the dimerization of three prototypic class I cytokine receptors in the plasma membrane of living cells by single-molecule fluorescence microscopy. Spatial and spatiotemporal correlation of individual receptor subunits showed ligand-induced dimerization and revealed that the associated Janus kinase 2 (JAK2) dimerizes through its pseudokinase domain. Oncogenic receptor and hyperactive JAK2 mutants promoted ligand-independent dimerization, highlighting the formation of receptor dimers as the switch responsible for signal activation. Atomistic modeling and molecular dynamics simulations based on a detailed energetic analysis of the interactions involved in dimerization yielded a mechanistic blueprint for homodimeric class I cytokine receptor activation and its dysregulation by individual mutations.</p