Current Biology最新文献

Itch is an aversive sensory experience inextricably linked to a desire to scratch.^1,2 While recent progress has advanced our understanding of itch sensation and transmission, the neural mechanisms underlying how scratching is sensed and controlled remain largely elusive. Here, we show that the left lateral habenula (LHb), which responds to negatively valent somatosensory stimuli,^3,4,5,6,7,8 preferentially engages and negatively regulates chloroquine (CQ)-evoked itch and scratching. Calcium activity in left LHb neurons increases when scratching is terminated, and their activation is sufficient to suppress itch-evoked scratching in an intensity-dependent manner. Peripheral MrgprD⁺ C-fiber afferents and PIEZO2 are required for scratching-evoked LHb activation and its suppression of scratching behaviors. Collectively, this work establishes a pathway that controls itch-evoked scratching from the periphery to the brain and reveals a novel left-right asymmetry of mammalian LHb functionality.

Calcium signaling in the vascular endothelium regulates vascular growth,^1,2 immune responses,³ and tone.⁴ Endothelial cells (ECs) are mechanosensitive,^5,6,7 and flow-driven shear stress is widely assumed to be the main trigger for EC Ca²⁺ responses in vivo.^8,9,10 Vascular ECs experience a range of distinct mechanical forces in vivo.^1,2,6,7 These include shear stress from blood flow, radial stretch from blood pressure, circumferential stretch from smooth-muscle-mediated vasodilation, and, in some parts of the animal, axial stretch from skeletal-muscle-mediated body motion^6,11 In principle, these different modes of stimulation could activate distinct signaling pathways and cellular responses.^12,13,14 Mechanical perturbation experiments on cultured cells or explants typically impose stresses that differ in magnitude and direction from the forces encountered in vivo,^5,15,16 and thus they cannot readily be used to assign biochemical responses to specific sources of mechanical stress in vivo. Here, we show that, in larval zebrafish, the dominant trigger for vascular endothelial Ca²⁺ events comes from body motion, not heartbeat-driven blood flow. Through a series of pharmacological and mechanical perturbations, we showed that body motion is necessary and sufficient to induce endothelial Ca²⁺ events, while neither neural activity nor blood circulation is necessary or sufficient. CRISPR-Cas9 knockout and temporally restricted photomorpholino knockdown identified Piezo1 as necessary for the rapid, mechanically evoked EC Ca²⁺ events.^10,17 Our results demonstrate that swimming-induced tissue motion is an important driver of endothelial Ca²⁺ dynamics in larval zebrafish.

Animal signals typically convey reliable information, but deception can evolve when the sender and receiver have conflicting interests-especially in the context of mating. Here, we provide evidence from a Cercopithecine primate, the gelada (Theropithecus gelada), that females deceptively signal fertility when conception is unlikely, which functions as a counterstrategy in sexual conflict. In geladas, male takeovers are frequent and often lead to sexually selected infanticide, exacting high costs on lactating females. Using 14 years of demographic and hormone data from wild geladas in Ethiopia, we show that lactating females quickly resumed sexual swellings and mated with the new male following takeovers, but they took significantly longer to conceive than females resuming cycling at other times. Females that exhibited these post-takeover swellings were subsequently less likely to lose their infants to infanticide. Fecal hormone data revealed a surge in estrogens after takeovers, even among females with the youngest infants, suggesting that estrogens mediate both fertile ("true") and non-fertile ("false") swellings. These results support the idea that sexual swellings can deceptively blur fertility as an adaptive counterstrategy to infanticide.

Immune cells are found in almost all animals, but their functions are well understood in very few. A new study in sea squirts shows that divergent paths are taken in immune cell evolution, even among members of our own phylum.

Monogenic expression of odorant receptors (ORs) in individual sensory neurons is a hallmark of olfactory systems in insects and vertebrates. New studies highlight how transcriptional interference and antisense transcription might ensure such selectivity in large OR arrays of social insects.

Appropriate classification of a novel stimulus as threatening or benign depends on a repertoire of prior environmental experiences involving challenge, risk, and opportunity^1,2. Without this library, individuals may classify harmless stimuli as dangerous - a hallmark of generalized anxiety^1,2. In humans, insufficient exposure to uncertainty or manageable risks is associated with heightened anxiety and maladaptive fear generalization and is theorized to contribute to rising rates of anxiety in children^3,4,5. Although animals in natural environments accumulate a wide range of experiences that allow them to calibrate threat assessment, most behavioral studies of anxiety rely on laboratory animals housed in static, impoverished conditions. In this laboratory context, the widely used elevated plus maze (a measure of anxiety) induces a persistent fear response in mice after a single exposure. Here we show that transferring adult mice from the lab to a large field enclosure mimicking natural mouse environments was sufficient to block the development of this fear response and restore baseline levels of anxiety behavior. A canonical rodent anxiety phenotype is thus environmentally contingent and rapidly reversible, underscoring the risks of inferring general behavioral principles from impoverished housing conditions.

Moreira et al. introduce aphelids, single-celled parasites of algae that kill their hosts during infection.

Organ morphogenesis requires tightly coordinated changes in cell shape and position, sometimes aided by transient cellular structures. In the C. elegans reproductive system, formation of the spermatheca-uterine valve involves a transient "core cell," but its function has remained unknown. Using long-term live imaging, cell-specific genetic perturbations, and biophysical assays, we show that the core cell mechanically guides valve morphogenesis through two mechanisms: it directs a sliding cell-cell junction that facilitates expansion of the valve's apical domain, and it promotes assembly of a contractile actomyosin network within the valve cell, essential for valve contraction and animal fertility. Ablation or softening of the transient core cell disrupted valve contractility and revealed a mechanical feedback loop in which resistance from the core cell reinforces actomyosin assembly in the valve. Our findings highlight how transient scaffold cells can coordinate morphogenesis in neighboring cells, ensuring precise and robust organ formation.

Sleep provides physiological benefits, but sleeping animals are unable to gain energy from foraging to fuel migration, self-maintenance, and reproduction¹. Therefore, trade-offs may exist between sleeping and foraging under energetic and ecological constraints^2,3. We use cutting-edge animal-borne sensors (bio-loggers) to show that northern elephant seals (Mirounga angustirostris) in poorer body condition have higher locomotory costs and exhibit less efficient foraging, which requires them to forage more and sleep less. Our results demonstrate that wild elephant seals can adjust their time-activity budgets to break out of a negative feedback loop of reduced fat stores and less efficient foraging, which likely promotes population persistence.