The goal of future quantum networks is to enable new internet applications that are impossible to achieve using only classical communication1-3. Up to now, demonstrations of quantum network applications4-6 and functionalities7-12 on quantum processors have been performed in ad hoc software that was specific to the experimental setup, programmed to perform one single task (the application experiment) directly into low-level control devices using expertise in experimental physics. Here we report on the design and implementation of an architecture capable of executing quantum network applications on quantum processors in platform-independent high-level software. We demonstrate the capability of the architecture to execute applications in high-level software by implementing it as a quantum network operating system-QNodeOS-and executing test programs, including a delegated computation from a client to a server13 on two quantum network nodes based on nitrogen-vacancy (NV) centres in diamond14,15. We show how our architecture allows us to maximize the use of quantum network hardware by multitasking different applications. Our architecture can be used to execute programs on any quantum processor platform corresponding to our system model, which we illustrate by demonstrating an extra driver for QNodeOS for a trapped-ion quantum network node based on a single 40Ca+ atom16. Our architecture lays the groundwork for computer science research in quantum network programming and paves the way for the development of software that can bring quantum network technology to society.

Nanoribbons, nanometre-wide strips of a two-dimensional material, are a unique system in condensed matter. They combine the exotic electronic structures of low-dimensional materials with an enhanced number of exposed edges, where phenomena including ultralong spin coherence times1,2, quantum confinement3 and topologically protected states4,5 can emerge. An exciting prospect for this material concept is the potential for both a tunable semiconducting electronic structure and magnetism along the nanoribbon edge, a key property for spin-based electronics such as (low-energy) non-volatile transistors6. Here we report the magnetic and semiconducting properties of phosphorene nanoribbons (PNRs). We demonstrate that at room temperature, films of PNRs show macroscopic magnetic properties arising from their edge, with internal fields of roughly 240 to 850 mT. In solution, a giant magnetic anisotropy enables the alignment of PNRs at sub-1-T fields. By leveraging this alignment effect, we discover that on photoexcitation, energy is rapidly funnelled to a state that is localized to the magnetic edge and coupled to a symmetry-forbidden edge phonon mode. Our results establish PNRs as a fascinating system for studying the interplay between magnetism and semiconducting ground states at room temperature and provide a stepping-stone towards using low-dimensional nanomaterials in quantum electronics.

Magnonic systems provide a fertile playground for bosonic topology1, for example, Dirac2-6 and Weyl7,8 magnons, leading to a variety of exotic phenomena such as charge-free topologically protected boundary modes6,7, the magnon thermal Hall effect9 and the magnon spin Nernst effect10. However, their understanding has been hindered by the absence of fundamental symmetry descriptions of magnetic geometries and spin Hamiltonians primarily governed by isotropic Heisenberg interactions. The ensuing magnon dispersions enable gapless magnon band nodes that go beyond the scenario of representation theory of the magnetic space groups11,12, thus referred to as unconventional magnons. Here we developed spin space group13-17 theory to elucidate collinear magnetic configurations, classifying the 1,421 collinear spin space groups into 4 types, constructing their band representations and providing a comprehensive tabulation of unconventional magnons, such as duodecuple points, octuple nodal lines and charge-4 octuple points. On the basis of the MAGNDATA database18, we identified 498 collinear magnets with unconventional magnons, among which more than 200 magnon band structures were obtained by using first-principles calculations and linear spin wave theory. In addition, we evaluated the influence of the spin-orbit-coupling-induced exchange interaction in these magnets and found that more than 80 per cent are predominantly governed by the Heisenberg interactions, indicating that the spin space group serves as an ideal framework for describing magnon band nodes in most 3d, 4d and half-filled 4f collinear magnets.

Global ocean surface temperatures were at record levels for more than a year from April 2023 onwards, exceeding the previous record in 2015-2016 by 0.25 °C on average between April 2023 and March 20241. The nearly global extent and unprecedented intensity of this event prompted questions about how exceptional it was and whether climate models can represent such record-shattering jumps in surface ocean temperatures2. Here we construct observation-based synthetic time series to show that a jump in global sea surface temperatures that breaks the previous record by at least 0.25 °C is a 1-in-512-year event under the current long-term warming trend (1-in-205-year to 1-in-1,185-year event; 95% confidence interval). Without a global warming trend, such an event would have been practically impossible. Using 270 simulations from a wide range of fully coupled climate models, we show that these models successfully simulate such record-shattering jumps in global ocean surface temperatures, underpinning the models' usefulness in understanding the characteristics, drivers and consequences of such events. These model simulations suggest that the record-shattering jump in surface ocean temperatures in 2023-2024 was an extreme event after which surface ocean temperatures are expected to revert to the expected long-term warming trend.

Intratumour heterogeneity and phenotypic plasticity drive tumour progression and therapy resistance1,2. Oncogene dosage variation contributes to cell-state transitions and phenotypic heterogeneity3, thereby providing a substrate for somatic evolution. Nonetheless, the genetic mechanisms underlying phenotypic heterogeneity are still poorly understood. Here we show that extrachromosomal DNA (ecDNA) is a major source of high-level focal amplification in key oncogenes and a major contributor of MYC heterogeneity in pancreatic ductal adenocarcinoma (PDAC). We demonstrate that ecDNAs drive varying levels of MYC dosage, depending on their regulatory landscape, enabling cancer cells to rapidly and reversibly adapt to microenvironmental changes. In the absence of selective pressure, a high ecDNA copy number imposes a substantial fitness cost on PDAC cells. We also show that MYC dosage affects cell morphology and dependence of cancer cells on stromal niche factors. Our work provides a detailed analysis of ecDNAs in PDAC and describes a new genetic mechanism driving MYC heterogeneity in PDAC.

Mechanical metamaterials with high recoverable elastic energy density, which we refer to as high-enthalpy elastic metamaterials, can offer many enhanced properties, including efficient mechanical energy storage1,2, load-bearing capability, impact resistance and motion agility. These qualities make them ideal for lightweight, miniaturized and multi-functional structures3-8. However, achieving high enthalpy is challenging, as it requires combining conflicting properties: high stiffness, high strength and large recoverable strain9-11. Here, to address this challenge, we construct high-enthalpy elastic metamaterials from freely rotatable chiral metacells. Compared with existing non-chiral lattices, the non-optimized chiral metamaterials simultaneously maintain high stiffness, sustain larger recoverable strain, offer a wider buckling plateau, improve the buckling strength by 5-10 times, enhance enthalpy by 2-160 times and increase energy per mass by 2-32 times. These improvements arise from torsional buckling deformation that is triggered by chirality and is absent in conventional metamaterials. This deformation mode stores considerable additional energy while having a minimal impact on peak stresses that define material failure. Our findings identify a mechanism and provide insight into the design of metamaterials and structures with high mechanical energy storage capacity, a fundamental and general problem of broad engineering interest.

Crop production faces persistent threats from insect-vector-borne viral diseases1,2. Recent advancements have revealed the intricate immune mechanisms that plants deploy against viral pathogens3-8. However, the molecular mechanisms through which plant hosts recognize viral infections and initiate antiviral defence at disease onset have not been elucidated. Here, through the natural infection of rice by inoculation with insect vectors carrying the natural forms of viruses, we show that viral coat proteins are perceived by the RING1-IBR-RING2-type ubiquitin ligase (RBRL), initiating the first step of the natural antiviral response in rice. RBRL subsequently targets an adaptor protein of the transcriptional repression complex of the jasmonate pathway, NOVEL INTERACTOR OF JAZ 3 (NINJA3), for degradation through the ubiquitination system, inducing jasmonate signalling and activating downstream antiviral defence. We further show that this phenomenon is a universal molecular mechanism used by rice plants to perceive viral infections and initiate antiviral signalling cascades. This approach is important not only for obtaining a deeper understanding of virus-host interactions but also for further disease resistance breeding.

In a subset of children and adolescents, SARS-CoV-2 infection induces a severe acute hyperinflammatory shock1 termed multisystem inflammatory syndrome in children (MIS-C) at four to eight weeks after infection. MIS-C is characterized by a specific T cell expansion2 and systemic hyperinflammation3. The pathogenesis of MIS-C remains largely unknown. Here we show that acute MIS-C is characterized by impaired reactivation of virus-reactive memory T cells, which depends on increased serum levels of the cytokine TGFβ resembling those that occur during severe COVID-19 (refs. 4,5). This functional impairment in T cell reactivity is accompanied by the presence of TGFβ-response signatures in T cells, B cells and monocytes along with reduced antigen-presentation capabilities of monocytes, and can be reversed by blocking TGFβ. Furthermore, T cell receptor repertoires of patients with MIS-C exhibit expansion of T cells expressing TCRVβ21.3, resembling Epstein-Barr virus (EBV)-reactive T cell clones capable of eliminating EBV-infected B cells. Additionally, serum TGFβ in patients with MIS-C can trigger EBV reactivation, which is reversible with TGFβ blockade. Clinically, the TGFβ-induced defect in T cell reactivity correlates with a higher EBV seroprevalence in patients with MIS-C compared with age-matched controls, along with the occurrence of EBV reactivation. Our findings establish a connection between SARS-CoV-2 infection and COVID-19 sequelae in children, in which impaired T cell cytotoxicity triggered by TGFβ overproduction leads to EBV reactivation and subsequent hyperinflammation.

Climate change is expected to increase heavy rainfall with concomitant increases in flooding1. Causes of increased heavy rainfall include the higher water-holding capacity of a warmer atmosphere and changes in atmospheric circulation patterns2, which may translate into future heavy rainfall increases in most of Europe3. However, gathering evidence on the time evolution of past changes has been hampered by data limitations and measurement uncertainties, in particular for short rainfall durations, such as 1 h. Here we show an 8% increase in daily and 15% increase in hourly heavy rainfall over the last four decades by analysing a new dataset comprising 883 stations in Austria from 1900 to 2023. These increases are fully consistent between two independent networks and occurred after a retarding phase between 1960 and 1980. Hourly heavy rainfall changes are aligned with temperature increases with the sensitivity of a 7% increase per 1 °C of warming, in line with Clausius-Clapeyron scaling. Daily heavy rainfall changes, however, are aligned with atmospheric circulation indices with little correlation to air temperature, which suggests a bigger role of atmospheric circulation modes than previously thought. The daily heavy rainfall changes are remarkably consistent with observed flood increases of about 8% in large catchments. The hourly heavy rainfall changes are similarly consistent with flood changes in small catchments, although the flood increase is stronger (25% over the last four decades). Climate adaptation measures in flood management may therefore be more pressing for rivers draining smaller catchment areas than for large rivers.

State-of-the-art climate models project a substantial decline in precipitation for the Mediterranean region in the future1. Supporting this notion, several studies based on observed precipitation data spanning recent decades have suggested a decrease in Mediterranean precipitation2-4, with some attributing a large fraction of this change to anthropogenic influences3,5. Conversely, certain researchers have underlined that Mediterranean precipitation exhibits considerable spatiotemporal variability driven by atmospheric circulation patterns6,7 maintaining stationarity over the long term8,9. These conflicting perspectives underscore the need for a comprehensive assessment of precipitation changes in this region, given the profound social, economic and environmental implications. Here we show that Mediterranean precipitation has largely remained stationary from 1871 to 2020, albeit with significant multi-decadal and interannual variability. This conclusion is based on the most comprehensive dataset available for the region, encompassing over 23,000 stations across 27 countries. While trends can be identified for some periods and subregions, our findings attribute these trends primarily to atmospheric dynamics, which would be mostly linked to internal variability. Furthermore, our assessment reconciles the observed precipitation trends with Coupled Model Intercomparison Project Phase 6 model simulations, neither of which indicate a prevailing past precipitation trend in the region. The implications of our results extend to environmental, agricultural and water resources planning in one of the world's prominent climate change hotspots10.

Optical amplification, crucial for modern communication, primarily relies on erbium-doped fibre amplifiers (EDFAs)1,2. Yet, EDFAs only cover a portion of the low-loss spectrum of optical fibres. This has motivated the development of amplifiers operating beyond the erbium gain window. Pioneering work on optical parametric amplifiers (OPAs)3,4 using intrinsic third-order optical nonlinearity has led to demonstrations of increased channel capacity. OPAs offer high gain, can reach the 3-dB quantum limit for phase-preserving amplifiers and exhibit unidirectional operation. However, power requirements for highly nonlinear fibres3,5-8 or bulk waveguides9,10 have impeded their adoption. By contrast, OPAs based on integrated photonic circuits offer the advantages of substantially increased mode confinement and optical nonlinearity but have been limited in bandwidth11,12. We overcome this challenge by using low-loss gallium phosphide-on-silicon dioxide13-15 photonic integrated circuits (PICs) and attain up to 35 dB of parametric gain with waveguides only a few centimetres long in a compact footprint of 0.25 square millimetres. Fibre-to-fibre net gain exceeding 10 dB across an ultra-broad bandwidth of approximately 140 nm (that is, 17 THz) is achieved, with a threefold increase in the gain window compared with C-band EDFAs. We further demonstrate a high dynamic range for input signals, spanning six orders of magnitude, while maintaining a low noise figure. We exploit these performance characteristics to amplify coherent communication signals. This marks, to our knowledge, the first ultra-broadband, high-gain, continuous-wave amplification in a photonic chip, opening up new capabilities for next-generation integrated photonics.

Navigating social environments is a fundamental challenge for the brain. It has been established that the brain solves this problem, in part, by representing social information in an agent-centric manner; knowledge about others' abilities or attitudes is tagged to individuals such as 'oneself' or the 'other'1-6. This intuitive approach has informed the understanding of key nodes in the social parts of the brain, the dorsomedial prefrontal cortex (dmPFC) and the anterior cingulate cortex (ACC)7-9. However, the patterns or combinations in which individuals might interact with one another is as important as the identities of the individuals. Here, in four studies using functional magnetic resonance imaging, behavioural experiments and a social group decision-making task, we show that the dmPFC and ACC represent the combinatorial possibilities for social interaction afforded by a given situation, and that they do so in a compressed format resembling the basis functions used in spatial, visual and motor domains10-12. The basis functions align with social interaction types, as opposed to individual identities. Our results indicate that there are deep analogies between abstract neural coding schemes in the visual and motor domain and the construction of our sense of social identity.

Hepatic stellate cells (HSCs) have a central pathogenetic role in the development of liver fibrosis. However, their fibrosis-independent and homeostatic functions remain poorly understood1-5. Here we demonstrate that genetic depletion of HSCs changes WNT activity and zonation of hepatocytes, leading to marked alterations in liver regeneration, cytochrome P450 metabolism and injury. We identify R-spondin 3 (RSPO3), an HSC-enriched modulator of WNT signalling, as responsible for these hepatocyte-regulatory effects of HSCs. HSC-selective deletion of Rspo3 phenocopies the effects of HSC depletion on hepatocyte gene expression, zonation, liver size, regeneration and cytochrome P450-mediated detoxification, and exacerbates alcohol-associated and metabolic dysfunction-associated steatotic liver disease. RSPO3 expression decreases with HSC activation and is inversely associated with outcomes in patients with alcohol-associated and metabolic dysfunction-associated steatotic liver disease. These protective and hepatocyte-regulating functions of HSCs via RSPO3 resemble the R-spondin-expressing stromal niche in other organs and should be integrated into current therapeutic concepts.

Mergers of binary neutron stars emit signals in both the gravitational-wave (GW) and electromagnetic spectra. Famously, the 2017 multi-messenger observation of GW170817 (refs. 1,2) led to scientific discoveries across cosmology3, nuclear physics4-6 and gravity7. Central to these results were the sky localization and distance obtained from the GW data, which, in the case of GW170817, helped to identify the associated electromagnetic transient, AT 2017gfo (ref. 8), 11 h after the GW signal. Fast analysis of GW data is critical for directing time-sensitive electromagnetic observations. However, owing to challenges arising from the length and complexity of signals, it is often necessary to make approximations that sacrifice accuracy. Here we present a machine-learning framework that performs complete binary neutron star inference in just 1 s without making any such approximations. Our approach enhances multi-messenger observations by providing: (1) accurate localization even before the merger; (2) improved localization precision by around 30% compared to approximate low-latency methods; and (3) detailed information on luminosity distance, inclination and masses, which can be used to prioritize expensive telescope time. Additionally, the flexibility and reduced cost of our method open new opportunities for equation-of-state studies. Finally, we demonstrate that our method scales to long signals, up to an hour in length, thus serving as a blueprint for data analysis for next-generation ground- and space-based detectors.

Tropical deforestation was found to cause large reductions in precipitation using a range of observation-based datasets1. However, the limitations of satellite-based space-for-time statistical analysis have hindered understanding of the roles of reshaped mesoscale atmospheric circulation and regional precipitation recycling at different scales. These effects are considered nonlocal effects, which are distinct from the local effects governed by deforestation-induced reductions in evapotranspiration (ET). Here we show reversed precipitation responses to Amazon deforestation across wet and dry seasons. During the wet season, deforested grids experienced a noteworthy increase in precipitation (0.96 mm month-1 per percentage point forest loss), primarily attributed to enhanced mesoscale atmospheric circulation (that is, nonlocal effect). These nonlocal increases weaken with distance from deforested grids, leading to significant precipitation reductions in buffers beyond 60 km. Conversely, during the dry season, precipitation decreases in deforested grids and throughout all analysis buffers, with local effects from reduced ET dominating. Our findings highlight the intricate balance between local effects and nonlocal effects in driving deforestation-precipitation responses across different seasons and scales and emphasize the urgent need to address the rapid and extensive loss of forest in the Amazon region.

More than ten ergot alkaloids comprising both natural and semi-synthetic products are used to treat various diseases1,2. The central C ring forms the core pharmacophore for ergot alkaloids, giving them structural similarity to neurotransmitters, thus enabling their modulation of neurotransmitter receptors3. The haem catalase chanoclavine synthase (EasC) catalyses the construction of this ring through complex radical oxidative cyclization4. Unlike canonical catalases, which catalyse H2O2 disproportionation5,6, EasC and its homologues represent a broader class of catalases that catalyse O2-dependent radical reactions4,7. We have elucidated the structure of EasC by cryo-electron microscopy, revealing a nicotinamide adenine dinucleotide phosphate (reduced) (NADPH)-binding pocket and a haem pocket common to all haem catalases, with a unique homodimeric architecture that is, to our knowledge, previously unobserved. The substrate prechanoclavine unprecedentedly binds in the NADPH-binding pocket, instead of the previously suspected haem-binding pocket, and two pockets were connected by a slender tunnel. Contrary to the established mechanisms, EasC uses superoxide rather than the more generally used transient haem iron-oxygen complexes (such as compounds I, II and III)8,9, to mediate substrate transformation through superoxide-mediated cooperative catalysis of the two distant pockets. We propose that this reactive oxygen species mechanism could be widespread in metalloenzyme-catalysed reactions.

For decades, antigen presentation on major histocompatibility complex class I for T cell-mediated immunity has been considered the primary function of proteasome-derived peptides1,2. However, whether the products of proteasomal degradation play additional parts in mounting immune responses remains unknown. Antimicrobial peptides serve as a first line of defence against invading pathogens before the adaptive immune system responds. Although the protective function of antimicrobial peptides across numerous tissues is well established, the cellular mechanisms underlying their generation are not fully understood. Here we uncover a role for proteasomes in the constitutive and bacterial-induced generation of defence peptides that impede bacterial growth both in vitro and in vivo by disrupting bacterial membranes. In silico prediction of proteome-wide proteasomal cleavage identified hundreds of thousands of potential proteasome-derived defence peptides with cationic properties that may be generated en route to degradation to act as a first line of defence. Furthermore, bacterial infection induces changes in proteasome composition and function, including PSME3 recruitment and increased tryptic-like cleavage, enhancing antimicrobial activity. Beyond providing mechanistic insights into the role of proteasomes in cell-autonomous innate immunity, our study suggests that proteasome-cleaved peptides may have previously overlooked functions downstream of degradation. From a translational standpoint, identifying proteasome-derived defence peptides could provide an untapped source of natural antibiotics for biotechnological applications and therapeutic interventions in infectious diseases and immunocompromised conditions.

The phytohormone auxin (Aux) is a principal endogenous developmental signal in plants. It mediates transcriptional reprogramming by a well-established canonical signalling mechanism. TIR1/AFB auxin receptors are F-box subunits of an ubiquitin ligase complex; after auxin perception, they associate with Aux/IAA transcriptional repressors and ubiquitinate them for degradation, thus enabling the activation of auxin response factor (ARF) transcription factors1-3. Here we revise this paradigm by showing that without TIR1 adenylate cyclase (AC) activity4, auxin-induced degradation of Aux/IAAs is not sufficient to mediate the transcriptional auxin response. Abolishing the TIR1 AC activity does not affect auxin-induced degradation of Aux/IAAs but renders TIR1 non-functional in mediating transcriptional reprogramming and auxin-regulated development, including shoot, root, root hair growth and lateral root formation. Transgenic plants show that local cAMP production in the vicinity of the Aux/IAA-ARF complex by unrelated AC enzymes bypasses the need for auxin perception and is sufficient to induce ARF-mediated transcription. These discoveries revise the canonical model of auxin signalling and establish TIR1/AFB-produced cAMP as a second messenger essential for transcriptional reprograming.