Current Biology最新文献

Understanding the mechanisms underlying homeostatic sleep regulation is a central, unmet goal of sleep science. Our comprehension of such regulation in mammals has required recognizing distinct sleep stages. Drosophila melanogaster is an important genetic model system for studying sleep. Since the discovery of sleep-like states in the fly 25 years ago, the field has treated sleep as a unitary state consisting of any inactivity lasting 5 min or longer, despite convergent work suggesting the existence of multiple sleep states. Here, we establish that three distinct sleep states in flies can be classified based on simple inactivity duration criteria. We show that the daily initiation of these sleep states is temporally distinct, with long sleep occurring immediately following the largest daily period of wakefulness. We also report that the rebound in response to mechanical sleep deprivation is present only in long sleep and comes at the expense of shorter sleep states. Deprivation-induced decreases in shorter sleep states obscure homeostatic sleep rebound, but only when sleep is measured using traditional methods. We observe distinctly timed ultradian oscillations of fly sleep states, reminiscent of mammalian sleep cycles. Our results indicate that the recognition of such sleep states will be necessary to fully realize the promise of the Drosophila model system for identifying conserved genetic mechanisms underlying sleep regulation.

Flies, like vertebrates, preserve the spatial organization of visual input through axonal projections into the brain, a principle called retinotopy. The best-known developmental mechanisms for retinotopy are molecular gradients in the target regions, yet Drosophila photoreceptors can form retinotopic maps ectopically in wrong brain regions. We show that a temporal gradient of axonal growth plus selective adhesion between photoreceptor axons precisely preserves the cellular eye pattern. Each of the 800 single eyes, the ommatidia, form a bundle of six axons that are held in place by inter-bundle adhesion through the protocadherin Flamingo and preserve their intra-bundle organization through the adhesion molecule Sidekick. Computational modeling of axon terminals as selectively adhesive soft bodies in a developmental wave generates the retinotopic pattern, including the shapes of the postsynaptic lamina neurons, which emerge without explicit encoding. Hence, a temporal gradient and two adhesive forces can ensure retinotopic map formation without a target-derived mechanism. VIDEO ABSTRACT.

Interview with Ansgar Büschges, who studies the neural mechanisms of locomotion at the University of Cologne.

The current biodiversity landscape results from hundreds of millions of years of evolution, yet the accumulation of biodiversity has been punctuated by mass extinctions. A key question is how surviving lineages rebuilt diversity after extinction events. Here, we examine the morphological and taxonomic recovery of three clades (i.e., ammonoids, brachiopods, and ostracods) that experienced selective extinction during the Permian-Triassic mass extinction (PTME) event. Using a deep learning method-based tool for automatic extraction of morphological features, combined with quantitative taxonomic diversity measures, we find two main paths of biotic recovery following the PTME: refilling mode, in which ammonoids and brachiopods rebound in biodiversity by refilling the vacated morphospace with limited innovation, leading to a partial recovery of their previous disparity and taxonomic diversity, and expansion mode, in which ostracods underwent an adaptive radiation, with their morphospace expanding rapidly during the Early-Middle Triassic and then stabilizing post-Triassic. Their ecological niches expanded substantially during the post-Paleozoic, and their diversity exceeded its pre-extinction level during the Jurassic. These findings suggest that rapid morphological diversification could facilitate ecological expansion and thereby foster long-term growth in taxonomic diversity. The PTME played a fundamental role in reshaping marine ecosystem structure by triggering different recovery trajectories among survivors.

Microbial competition serves as a fundamental driver for the evolution of offensive and defensive mechanisms among microorganisms. While it is well established that bacteria utilize specialized secretion systems to deliver both toxic and non-toxic effector proteins into competing cells, thereby directly killing them or modulating cellular events, it remains largely unclear whether bacteria can hijack effector proteins derived from competitors to resolve interspecies conflicts. Here, we demonstrate that Pseudomonas protegens employs a sophisticated defense strategy, hijacking LtaE, a non-cytotoxic effector delivered via the type IV secretion system (T4SS) of non-flagellated Lysobacter enzymogenes, to resolve interbacterial conflict through transcriptional reprogramming. Translocated LtaE neutralizes an uncharacterized antibacterial toxin in P. protegens. Surprisingly, as a countermeasure, P. protegens hijacks LtaE to rewire its host signaling hierarchy, converting it into a motility activation switch. Mechanistically, LtaE directly binds to FleQ, the σ54-dependent master regulator of flagellar biosynthesis, shielding it from inhibitory c-di-guanosine monophosphate (GMP) binding-a universal second messenger whose elevated concentration typically inhibits bacterial motility and promotes biofilm formation. Remarkably, the LtaE-FleQ complex remains stable under high c-di-GMP conditions, overriding sessility signals to derepress flagellar gene expression and trigger escape motility. Biochemical analyses reveal that LtaE broadly targets FleQ homologs across pseudomonads through competitive inhibition of c-di-GMP binding, linking competitor detection to motility activation. Our findings establish a novel bacterial conflict-resolution paradigm, demonstrating how non-cytotoxic effectors act as molecular switches to dynamically reprogram transcriptional networks and enhance phenotypic plasticity.

Many animals strongly rely on vision, as it provides high-dimensional information about the natural world.¹ To extract relevant features, neural systems filter and categorize the visual input early on to reduce its complexity.² In insects, the first visual processing stage of the brain, the lamina neuropil, plays an important role in parallel processing.³ Its main relay neurons, lamina monopolar cells (LMCs),⁴ receive direct photoreceptor input and shape the contrast, luminance, and spatial and temporal tuning of the insect visual system in a cell-type-specific manner. However, how contrast and luminance processing is delineated by LMCs is known only from fruit flies,⁵ while the contribution of LMCs to spatial processing has been described in hawkmoths.⁶ Here, we reconcile the contrast, luminance, and spatial processing properties of LMCs feeding to the best-investigated downstream target, the motion pathway.⁷ To this aim, we provide a novel characterization of hawkmoth LMCs, using serial block-face scanning electron microscopy to reconstruct the anatomical fine structure and connectivity of LMCs in a focal lamina cartridge. We further characterized the functional properties of the main relay neurons (L1 and L2) to the motion pathway in terms of contrast and spatial processing. Crucially, their two distinct spatial processing functions, lateral inhibition and spatial summation, are explained by the density and distribution of their synapses in different lamina layers. Based on these findings, we propose a novel mechanism of delineating distinct spatial processing functions in a single cell.

Endoplasmic reticulum (ER) stress and the hypersensitive response (HR) are recognized as cornerstones of plant immunity; however, the mechanistic synergy and the strategies pathogens employ to dismantle this alliance remain elusive. Here, we identify a virulence effector, PstCRT (calreticulin), from Puccinia striiformis f. sp. tritici (Pst), that suppresses host immune responses by disrupting ER stress-mediated HR. PstCRT directly targets the HR-like lesion-inducing protein (TaHRLI) in wheat and obstructs its ER translocation. Within the ER lumen, TaHRLI interacts with wheat calreticulin (TaCRT), triggering Ca²⁺ efflux and activating the unfolded protein response (UPR) to induce cell death and disease resistance. Pathogen-derived PstCRT structurally mimics TaCRT to sequester TaHRLI to the plasma membrane via competitive interaction, thereby effectively suppressing ER stress-induced HR initiation. Crucially, we found that CRT secretion represents a conserved virulence strategy across different rust genera. AlphaFold-guided engineering of TaHRLI in wheat generated the TaHRLI^Mut variant that evades PstCRT recognition. Overexpressing TaHRLI^Mut in wheat conferred broad-spectrum resistance against Pst in biennial field trials, effectively mitigating pathogen-induced yield losses while preserving essential agronomic traits. Collectively, this study elucidates a molecular mechanism underlying pathogen disruption of ER stress-induced HR to promote infection and proposes an innovative strategy for engineering durable crop protection.

Although migration is widespread among many animal taxa, including ungulates,¹ the fitness benefits associated with different migratory tactics have rarely been documented.^2,3 Here, we evaluated a 9-year dataset on a migratory population of mule deer in western North America to understand whether long-distance migration provides access to seasonal forage, which translates into demographic benefits. Mule deer that migrated over 50 km to high-elevation summer ranges accessed higher forage quality and thus gained around twice the amount of fat over the growing season compared with mule deer that remained year-round as residents within a desert ecosystem. Elevated levels of fat translated to ∼20% higher probability of adult annual survival than residents. Mule deer that remained year-round in the desert portion of the study area were so resource-limited that they raised fawns at the expense of their own survival. Due to their higher levels of fat, annual survival, and fetal rates, migrants showed more robust population growth (λ = 1.03) compared to residents, which exhibited projected declines in population size over time (λ = 0.95). These results support the notion that migration translates into demographic benefits and highlight the urgent conservation work necessary to sustain diverse ungulate migrations amid habitat alteration due to climate change and an expanding web of linear barriers to movement.^3,4,5.

Recalling the past is crucial for shaping the present and planning for the future. Yet, some memories are better to be forgotten. A new study sheds light on an unconventional mechanism to devalue learned memories.

Intrinsic enteric neurons regulate gut motility, secretion, and absorption, whereas extrinsic dorsal root ganglia sensory neurons are key in colon interoception and visceral pain. A new study raises the question of whether some initial interoceptive signals could originate from enteric neurons.