Global S&T Development Trend Analysis Platform of Resources and Environment
Carbonaceous (C-type) asteroids(1) are relics of the early Solar System that have preserved primitive materials since their formation approximately 4.6 billion years ago. They are probably analogues of carbonaceous chondrites(2,3) and are essential for understanding planetary formation processes. However, their physical properties remain poorly known because carbonaceous chondrite meteoroids tend not to survive entry to Earth'
Thermal imaging data obtained from the spacecraft Hayabusa2 reveal that the carbonaceous asteroid 162173 Ryugu is an object of unusually high porosity.
The ability to communicate quantum information over long distances is of central importance in quantum science and engineering(1). Although some applications of quantum communication such as secure quantum key distribution(2,3) are already being successfully deployed(4-7), their range is currently limited by photon losses and cannot be extended using straightforward measure-and-repeat strategies without compromising unconditional security(8). Alternatively, quantum repeaters(9), which utilize intermediate quantum memory nodes and error correction techniques, can extend the range of quantum channels. However, their implementation remains an outstanding challenge(10-16), requiring a combination of efficient and high-fidelity quantum memories, gate operations, and measurements. Here we use a single solid-state spin memory integrated in a nanophotonic diamond resonator(17-19) to implement asynchronous photonic Bell-state measurements, which are a key component of quantum repeaters. In a proof-of-principle experiment, we demonstrate high-fidelity operation that effectively enables quantum communication at a rate that surpasses the ideal loss-equivalent direct-transmission method while operating at megahertz clock speeds. These results represent a crucial step towards practical quantum repeaters and large-scale quantum networks(20,21).
A solid-state spin memory is used to demonstrate quantum repeater functionality, which has the potential to overcome photon losses involved in long-distance transmission of quantum information.
Hydrogen peroxide (H2O2) is a major reactive oxygen species in unicellular and multicellular organisms, and is produced extracellularly in response to external stresses and internal cues(1-4). H2O2 enters cells through aquaporin membrane proteins and covalently modifies cytoplasmic proteins to regulate signalling and cellular processes. However, whether sensors for H2O2 also exist on the cell surface remains unknown. In plant cells, H2O2 triggers an influx of Ca2+ ions, which is thought to be involved in H2O2 sensing and signalling. Here, by using forward genetic screens based on Ca2+ imaging, we isolated hydrogen-peroxide-induced Ca(2+)increases (hpca) mutants in Arabidopsis, and identified HPCA1 as a leucine-rich-repeat receptor kinase belonging to a previously uncharacterized subfamily that features two extra pairs of cysteine residues in the extracellular domain. HPCA1 is localized to the plasma membrane and is activated by H2O2 via covalent modification of extracellular cysteine residues, which leads to autophosphorylation of HPCA1. HPCA1 mediates H2O2-induced activation of Ca2+ channels in guard cells and is required for stomatal closure. Our findings help to identify how the perception of extracellular H2O2 is integrated with responses to various external stresses and internal cues in plants, and have implications for the design of crops with enhanced fitness.
HPCA1, a member of a previously uncharacterized subfamily of leucine-rich-repeat receptor-like kinases, is the hydrogen-peroxide sensor at the plasma membrane in Arabidopsis.
Epithelial-to-mesenchymal transitions (EMTs) are phenotypic plasticity processes that confer migratory and invasive properties to epithelial cells during development, wound-healing, fibrosis and cancer(1-4). EMTs are driven by SNAIL, ZEB and TWIST transcription factors(5,6) together with microRNAs that balance this regulatory network(7,8). Transforming growth factor beta (TGF-beta) is a potent inducer of developmental and fibrogenic EMTs4,9,10. Aberrant TGF-beta signalling and EMT are implicated in the pathogenesis of renal fibrosis, alcoholic liver disease, non-alcoholic steatohepatitis, pulmonary fibrosis and cancer(4,11). TGF-beta depends on RAS and mitogen-activated protein kinase (MAPK) pathway inputs for the induction of EMTs12-19. Here we show how these signals coordinately trigger EMTs and integrate them with broader pathophysiological processes. We identify RAS-responsive element binding protein 1 (RREB1), a RAS transcriptional effector(20,21), as a key partner of TGF-beta-activated SMAD transcription factors in EMT. MAPK-activated RREB1 recruits TGF-beta-activated SMAD factors to SNAIL. Context-dependent chromatin accessibility dictates the ability of RREB1 and SMAD to activate additional genes that determine the nature of the resulting EMT. In carcinoma cells, TGF-beta-SMAD and RREB1 directly drive expression of SNAIL and fibrogenic factors stimulating myofibroblasts, promoting intratumoral fibrosis and supporting tumour growth. In mouse epiblast progenitors, Nodal-SMAD and RREB1 combine to induce expression of SNAIL and mesendoderm-differentiation genes that drive gastrulation. Thus, RREB1 provides a molecular link between RAS and TGF-beta pathways for coordinated induction of developmental and fibrogenic EMTs. These insights increase our understanding of the regulation of epithelial plasticity and its pathophysiological consequences in development, fibrosis and cancer.
RAS and TGF-beta pathways regulate distinct modes of epithelial-to-mesenchymal transition via RAS-responsive element binding protein 1.
Analysis of metagenomics data revealed that large and giant viruses are globally widely distributed and are associated with most major eukaryotic lineages.
Our current knowledge about nucleocytoplasmic large DNA viruses (NCLDVs) is largely derived from viral isolates that are co-cultivated with protists and algae. Here we reconstructed 2,074 NCLDV genomes from sampling sites across the globe by building on the rapidly increasing amount of publicly available metagenome data. This led to an 11-fold increase in phylogenetic diversity and a parallel 10-fold expansion in functional diversity. Analysis of 58,023 major capsid proteins from large and giant viruses using metagenomic data revealed the global distribution patterns and cosmopolitan nature of these viruses. The discovered viral genomes encoded a wide range of proteins with putative roles in photosynthesis and diverse substrate transport processes, indicating that host reprogramming is probably a common strategy in the NCLDVs. Furthermore, inferences of horizontal gene transfer connected viral lineages to diverse eukaryotic hosts. We anticipate that the global diversity of NCLDVs that we describe here will establish giant viruses-which are associated with most major eukaryotic lineages-as important players in ecosystems across Earth'