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Reply to Topaz and Bahl: Interpreting a post-2022 lexical shift in academic prose

Correction for Wu et al., Paramyxovirus infection driven by heteromultivalent sialoglycotope binding

Heat tolerance decreases and cold tolerance increases with elevation for a species-rich insect family on a tropical volcano

The climate crisis is moving the high ambient temperatures common in lower elevation tropical forests upslope into areas where they would not have occurred historically. Tropical invertebrates may be particularly vulnerable to such changes. Here, our goal was to understand whether the distribution of heat and cold tolerances along an elevational gradient in northwestern Costa Rica predicted by theory were present for a leaf-litter inhabiting insect community of rove beetles (Staphylinidae: Coleoptera). We found that heat tolerance decreased, and cold tolerance increased with elevation, supporting the predictions. High elevation communities may not be capable of tolerating the rising temperatures that come with climate change, while low elevation communities are already experiencing environmental temperatures that may meet or exceed their thermal limits. While the forests in the low elevation more frequently exhibit temperatures that meet or exceed the heat tolerances for the beetle community, the soil will offer a buffered refuge for some time. The decline in thermal tolerance that we show here is predicted by theory yet is inconsistent with the values for insect species in the thermal tolerance literature. This reinforces the need for a better understanding of the thermal tolerances of diverse assemblages of tropical species that are likely to experience complicated and negative impacts of climate change.

PLCβs are recruited to the plasma membrane in macrophages by both Gβγ and Gα _q

PLCβ enzymes cleave PIP2 from the plasma membrane, producing IP3 and DAG, which regulate intracellular Ca 2+ levels and protein kinase C activity, respectively. They are regulated by GPCR signaling through the G proteins Gβγ and Gα q and have been shown to function as coincidence detectors for dual stimulation of Gα q - and Gα i -coupled receptors via these G proteins. PLCβs are aqueous-soluble enzymes, but partition onto the membrane surface to access their lipid substrate. We previously demonstrated that membrane recruitment and orientation of the catalytic core on the membrane surface underlie Gβγ-dependent regulation of PLCβ enzymes. Using macrophages as a model system, where PLCβ signaling is essential for responses to infection and tissue injury, we investigated the contribution of Gβγ-dependent regulation and membrane recruitment of PLCβ in the context of endogenous signaling. By measuring Ca 2+ mobilization, we demonstrate that both Gα i - and Gα q -coupled receptors independently stimulate PLCβ activity. Using total internal reflection fluorescence and stimulated emission depletion microscopy, we demonstrate that most of the PLCβ3 in the cell is localized away from the plasma membrane at rest but is rapidly recruited to the plasma membrane upon stimulation by both Gα i - and Gα q -coupled receptors, illustrating that both Gβγ and Gα q recruit PLCβ to the plasma membrane. These results support an updated model for G protein–dependent regulation of PLCβ enzymes, where Gβγ-induced regulation in the absence of Gα q can occur and is apparently dictated by the local concentration of receptor, G proteins, and PLCβ.

When coordination is avoidable: A monotonicity analysis of organizational tasks

Organizations devote substantial resources to coordination, yet which tasks actually require it for correctness remains unclear. The problem is acute in multiagent AI systems, where coordination cost is directly measurable and can exceed the cost of the work itself. Distributed systems theory provides a precise criterion: Coordination is required when a task specification is nonmonotonic, meaning that as histories grow, new information can invalidate prior conclusions. Here we show that Thompson’s classic taxonomy of interdependence maps to that criterion, yielding a decision rule for when coordination is required for correctness. We formalize the correspondence in a bridge theorem, apply the rule to 65 workflows from the American Productivity & Quality Center (APQC), and (with a calibrated large language model (LLM), 13,417 Occupational Information Network (O*NET tasks), and illustrate it in multiagent AI simulations. Under our decompositions, 74% of workflows and 42% of O*NET tasks are monotonic, implying that up to 24 to 57% of coordination spending is unnecessary for correctness.

Sources of technological innovation

Correction for Meng et al., Rethinking energy transition strategies for the European Union amid rising energy prices

Lexical change is not a calibrated measure of LLM prevalence or its determinants

PLK1-mediated phosphorylation of PHGDH reprograms serine metabolism in advanced prostate cancer

Metabolic reprogramming is a hallmark of cancer, enabling tumor cells to meet their increased biosynthetic and energetic demands. Although cells possess the capacity for de novo serine biosynthesis, most transformed cancer cells preferentially rely on exogenous serine uptake to sustain their growth, yet the regulatory mechanisms driving this metabolic dependency remain poorly understood. Here, we uncover a mechanism by which Polo-like kinase 1 (PLK1), frequently overexpressed in prostate cancer, orchestrates a metabolic shift in serine and sphingolipid metabolism through phosphorylation of phosphoglycerate dehydrogenase (PHGDH), the rate-limiting enzyme of the serine synthesis pathway (SSP). Specifically, PLK1 directly phosphorylates PHGDH at S512, S513, and S517, leading to a marked reduction in its protein level and enzymatic activity. This downregulation of de novo serine biosynthesis forces cancer cells to increase their reliance on exogenous serine uptake via the ASCT2 transporter, which in turn fuels the biosynthesis of lipids, including sphingolipids essential for tumor growth and survival. Our findings suggest that targeting the SSP, serine uptake, or downstream lipid biosynthesis pathways may represent promising therapeutic strategies in advanced cancers characterized by PLK1 dysregulation.

Insights into hominin body size, locomotion, and behavior from Early Pleistocene trackways in northern Kenya

The Early Pleistocene fossils of the Koobi Fora Formation, northern Kenya, record two well-documented hominin genera, Homo and Paranthropus , preserved in the same deposits. Evidence for their ecological sympatry consists of co-occurring footprints of diverse morphologies, suggesting that Homo erectus and Paranthropus boisei were present in the same lake margin habitats over hundreds of thousands of years. Here, we report on a ~1.43 Ma fossil footprint assemblage that sheds light on Early Pleistocene hominin paleobiology and behavior. The internal morphologies of the hominin tracks align with others previously attributed to P. boisei , indicating patterns of foot morphology and locomotion different from modern Homo and more consistent with those seen in earlier Australopithecus species. However, the tracks indicate body sizes that exceed the largest skeletal estimates for P. boisei , raising the possibility that they may belong to H. erectus . Depending on their attribution, the tracks demonstrate a) larger body sizes and greater size variation in P. boisei than previously recognized, or b) levels of intraspecific anatomical and locomotor variation in H. erectus that far exceed those yet observed in modern humans or other fossil taxa. Regardless of their attribution, these tracks indicate larger than average body sizes. This supports the hypothesis that they capture a group that included multiple adult males and offers rare direct evidence for hominin social behavior. The ecological context of the tracks suggests that hominins were accessing resources in a deltaic lake margin habitat.

ICE arrests, 2015–2026: Variation in targeting, method, and geography

We analyze and decompose administrative data on all 1.6 million US Immigration and Customs Enforcement (ICE) arrests from October 2015 to March 2026. Our results reveal that the reality of immigration enforcement diverges sharply from the public narrative that ICE arrests are necessary to protect public safety by removing people who commit crimes: Although arrests spiked at the outset of both Trump presidencies, the share of arrested individuals with criminal convictions fell significantly, with especially marked declines in 2025. A shift in ICE tactics partly explains this pattern, but even conditional on tactic, the share with a criminal conviction declined as arrests rose. Moreover, we find substantial geographic heterogeneity in ICE methods, despite nearly universal declines in the criminal conviction rate. Our findings provide important evidence for policymakers, the general public, and researchers studying this period of immigration policy.

MORC2 controls HIF-1α stability via an HDAC4-dependent mechanism to regulate erythropoiesis

The hypoxia-inducible factor (HIF) signaling pathway is essential for cellular adaptation to low oxygen. Although the canonical PHD-pVHL pathway that mediates HIF-α degradation under normoxia is well established, alternative regulatory mechanisms remain poorly understood. Here, we identify Microrchidia family CW-type zinc-finger 2 (MORC2) as a negative regulator of HIF-α. In zebrafish, CRISPR/Cas9-generated morc2 mutants developed polycythemia, systemic hypoxia, and constitutive activation of the HIF pathway. Mechanistically, MORC2 counteracts histone deacetylase 4 (HDAC4) by competing for HIF-1α binding. Loss of MORC2 enhances HDAC4 recruitment to HIF-1α, reducing acetylation at lysine 629 and preventing proteasomal degradation of HIF-1α. These results define a regulatory mechanism in which MORC2 modulates HIF-1α stability via HDAC4 mediated deacetylation, shedding light on hematopoiesis and HIF-related disorders.

Palindrome in the sequence of the ribosomal peptidyl transferase center suggests a protoribosome emergence scheme

The emergence of a simple version of the modern ribosome represents an indispensable step in the evolution of life as we know it. Standalone dimeric protoribosome models, derived from the peptidyl transferase center of the modern ribosome, have been shown to perform the primary ribosomal function of catalyzing peptide bond formation. However, the likelihood of the random occurrence of a suitable 70-mer RNA strand capable of serving as the monomer sequence remains questionable. Here, what initially appeared to be a “hallucinatory” AlphaFold3 prediction of a putative protoribosome, was found to express the presence of a palindrome spanning most of the ribosome-derived monomer sequence. The framework of this sequence suggests a simple, experimentally testable molecular mechanism by which an analog of the ribosome-derived protoribosome could have self-assembled from a few copies and complementary strands of a single 10-mer RNA segment. This scenario significantly reduces the complexity attributed to the autonomous emergence of a protoribosome and provides a plausible starting point for a continuous evolutionary pathway, leading from inanimate matter to life as we know it.

Reply to Szöllősi and Williams: The observation threshold mitigates the bias of transient genes on ancestral reconstruction

Sprint-like cardiac dynamics support repeated acrobatic lunges in foraging rorqual whales

The dive response decreases heart rate, regulates blood flow distribution, conserves oxygen, and extends dive duration. In diving animals, dive heart rate can be modulated to meet increased demands of exercise during foraging. However, lunge-feeding rorquals represent an extreme example of exercise under breath-hold conditions: Though most of their dive time is spent gliding and filtering, lunges require high-power, acrobatic sprints to engulf massive volumes of prey-laden water. Our biologging data show that heart rate repeatedly increases with lunging but only gradually declines during filtering, dissimilar from the heart rate-activity coupling observed in other divers. We suggest that the unique nature of rorqual exercise likely requires glycolytic metabolic substrates, rather than aerobic substrates, during short, powerful lunges. During slow filtering, high heart rates may help partially renew these energy sources via oxygen-dependent pathways. By temporarily buffering oxygen demand from supply, the flexible dive response appears to optimize oxygen use in lunging rorquals and support aerobically “cheap” foraging. The data also show that dive cycle heart rate scope increases with rorqual size. We propose that cardiovascular plasticity during high and low power phases of foraging dives underpins rorquals’ ability to achieve high foraging efficiencies and combine explosive predation with grazing-like efficiency in a single lineage.

Methionine oxidation alters both helical assembly and disordered contacts in human TDP-43 C-terminal domain phase separation

TAR DNA binding protein 43 (TDP-43), a key protein linked to ALS pathology, undergoes phase separation and forms functional assemblies via condensation within cells. The conserved region (CR) within its C-terminal domain (CTD) mediates self-assembly through helix–helix interactions, while the flanking intrinsically disordered regions (IDRs) contribute to phase separation through transient interactions involving aromatic and hydrophobic residues. The CTD contains ten methionine residues distributed equally between these regions, making it particularly susceptible to oxidative modifications. While methionine oxidation is known to impair TDP-43 phase separation, neither the precise mechanism nor the specific contribution of methionines in the CR compared to the IDRs has been determined. Here, we combine NMR spectroscopy and molecular dynamics (MD) simulations to reveal if and how methionine oxidation in each region differentially affects CTD structure and phase separation. To assess the change of secondary structure caused by oxidation, we measured NMR random coil chemical shift values for methionine sulfoxide. Oxidation of CR methionines disrupts helical structure and directly impairs intermolecular helical association, while oxidation of IDR methionines disrupts long-range contacts. Hence, oxidation of methionines in both regions contributes to impaired phase separation, albeit through different mechanisms. These findings establish methionines as critical redox-sensitive modulators in TDP-43 phase behavior and provide molecular insights into how oxidative stress may contribute to TDP-43 dysregulation in neurodegenerative diseases.

Going in reverse to get it right in RNA replication

Correction for Zhang et al., Programmable DNA hydrogels for dual-mode PD-L1 suppression via polyvalent LYTAC mimics and transcriptional silencing

Christopher A. Sims (1942–2026): Paradigm-shifting macroeconomist and econometrician

Christopher A. Sims, who died on March 14, 2026, left behind an indelible mark on macroeconomics and econometrics. His Nobel Prize winning research reshaped the paradigm for empirical macroeconomics, creating a rigorous and flexible framework for inferring the effects of macroeconomic policies. He also made important contributions to time series forecasting, Bayesian econometrics, factor modeling, approximation theory, and models of monetary and fiscal policy. Few academics have had as direct an impact on the work of central banks throughout the world. A frank and generous mentor with numerous students, Chris’s impact extends well beyond his published papers.

Reversing vegetable biodiversity loss to diversify diets

Vegetables are a critical component of diets, with inadequate intake of this essential food group leading to poor dietary quality and malnutrition. Food system assessments identify insufficient production, comparatively high prices, and sociocultural barriers as key constraints to vegetable consumption. We argue that vegetable biodiversity, spanning vegetable species and their varieties, as well as their wild relative species, is a central yet underutilized lever for enhancing vegetable consumption. Vegetables span a wider phylogenetic range than any other plant-derived food group, offering options for different climatic, cultural, and market niches worldwide. However, vegetable biodiversity is declining due to market homogenization, land-use change, and other threats. Its current conservation is insufficient, restricting in turn access to this diversity for research, breeding, and innovation, and making it more difficult to bridge the gap between current and recommended vegetable intake. Reversing this trend globally requires aligning conservation with dietary goals through four complementary action areas: i) Securing vegetable biodiversity by collecting, regenerating, and conserving local crop varieties and wild relatives of key vegetable species in biodiversity hotspots; ii) Harnessing vegetable biodiversity to deliver new varieties through collaborative research, breeding, and variety testing; iii) Promoting vegetable biodiversity to diversify diets, particularly among children and other vulnerable groups, by including nutrient-dense, climate-resilient vegetables into home and school meals; and iv) Integrating vegetable biodiversity into policy frameworks for long-term impact. Implementing this integrated approach in hotspots where vegetable biodiversity and malnutrition overlap can transform an overlooked opportunity into a cornerstone strategy for healthier diets.