Current Biology最新文献

After the Permian-Triassic mass extinction, surviving lineages recovered in different ways. A new study reveals specific recovery trajectories in three different marine groups, some of which refilled lost morphological disparity while others exploited extinction-driven opportunities to innovate.

Humans and animals learn about the world through targeted and deliberate movement of the head, eyes, hands, and other sensors. A new study demonstrates how the geometry of the rat whisker system simplifies the motor control of active sensing.

Cell wall patterning plays a crucial role in determining the function of plant cells.¹ Protoxylem and metaxylem vessel cells form striped and pitted cell walls, respectively, to facilitate efficient water transport.^2,3,4 These patterned cell walls are deposited beneath the cortical microtubules.^5,6 The microtubule depletion domain 1 (MIDD1) pathway removes cortical microtubules to promote cell wall spacing in xylem vessels,^7,8,9 but overall, the regulatory network of cell wall patterning in xylem vessels and its links with external signals remain poorly understood. Here, we show that acetylated interacting protein 1 (ACIP1), the target of the bacterial type III effector, inhibits cell wall spacing in protoxylem vessels. An acip1 loss-of-function mutant displayed abnormally wide cell wall spacing, while ACIP1 overexpression resulted in narrower cell wall spacing. Additive phenotypes were observed when ACIP1 was knocked out or overexpressed in midd1 midd2 plants, suggesting that ACIP1 functions independently of the MIDD1 pathway. ACIP1 localized to microtubules in vitro. Overexpression of ACIP1 caused bundling and longitudinal rearrangement of cortical microtubules in the epidermis, suggesting that ACIP1 acted via microtubules as a negative regulator of cell wall spacing in protoxylem vessels, thereby counteracting the MIDD1 pathway. These findings reveal a novel mechanism in which two pathways, ACIP1 and MIDD1, act in opposition to coordinate cell wall patterning in protoxylem vessels, suggesting a potential link between xylem architecture and plant immunity.

Assigning valence-appeal or aversion-to gustatory stimuli and relaying it to higher-order brain regions to guide flexible behaviors is crucial to survival. Yet the neural circuits that transform taste into motivationally relevant signals remain poorly defined in any model system. In Drosophila melanogaster, substantial progress has been made in mapping the sensorimotor pathways encoding intrinsic valence for feeding and the architecture of the dopaminergic reinforcement system. However, where and how "effective" (i.e., real-time) valence is first imposed on a taste has long been a mystery. Here, we identified a pair of subesophageal zone interneurons in Drosophila, termed Fox, that impart reinforcing positive valence to sweet taste and convey this signal to the mushroom body, the fly's associative learning center. We show that Fox neuron activity is necessary and sufficient to drive appetitive behaviors and can override a tastant's intrinsic neutral or aversive valence without impairing taste quality discrimination. Furthermore, Fox neurons relay the positive valence to specific dopaminergic neurons that mediate appetitive memory formation. Our findings reveal a circuit mechanism through which effective valence is bestowed upon sweet sensation and transformed into a reinforcing signal that supports learned sugar responses. The Fox neurons form a convergent-divergent "hourglass" circuit motif, acting as a bottleneck for valence assignment and distributing motivational signals to higher-order centers. This architecture confers both robustness and flexibility in reward processing-an organizational principle that may generalize across species.

Alzheimer's disease is characterized by progressive memory decline associated with hippocampal degeneration. However, the specific physiological mechanisms underlying hippocampal dysfunction in the disease remain poorly understood-improved knowledge may aid diagnosis and identify new avenues for therapeutic intervention. We investigated how disruptions in hippocampal reactivations relate to place cell stability and spatial memory deficits in an Alzheimer's mouse model. Using the App knockin mouse model NL-G-F, we conducted simultaneous behavioral and electrophysiological recordings in a radial arm maze. NL-G-F mice exhibited significant impairments in memory performance, demonstrated by an increased propensity to revisit arms, compared with wild-type controls. These memory deficits were associated with reduced stability of hippocampal place cells, which was particularly pronounced following rest periods. Crucially, although wild-type mice showed enhanced place cell stability after quiescence, NL-G-F mice failed to exhibit this consolidation. Although the rate of hippocampal reactivation events during rest remained unchanged, analysis of replay content revealed significantly degraded replay quality in NL-G-F mice. This degradation manifested as disrupted cell recruitment and reduced co-firing structure within reactivation events, both of which predicted the failure of offline place cell stabilization. Together, these findings suggest that compromised reactivation quality may underlie disruptions in offline consolidation processes, offering a potential mechanism for memory dysfunction in Alzheimer's disease.

Neurons continuously adjust their properties as a function of experience. Precise modulation of neuronal responses is achieved by multiple cellular mechanisms that operate over a range of timescales. Primary sensory neurons not only rapidly adapt their sensitivities via posttranslational mechanisms, including regulated trafficking of sensory molecules,^1,2,3,4 but also alter their transcriptional profiles on longer timescales to adapt to persistent sensory stimuli.^5,6,7,8 How diverse transcriptional and posttranscriptional pathways are coordinated in individual sensory neurons to accurately adjust their functions and drive behavioral plasticity is unclear. Here, we show that temperature experience modulates both transcription and trafficking of thermoreceptors on different timescales in the C. elegans AFD thermosensory neurons to regulate response plasticity. Expression of the PY motif-containing adaptor protein (PY motif transmembrane 1 [PYT-1]), as well as the GCY-18 warm temperature-responsive guanylyl cyclase thermoreceptor,⁹ is transcriptionally upregulated in AFD upon a temperature upshift.^5,10 We find that as GCY-18 begins to accumulate at the AFD sensory endings, the GCY-23 cooler temperature-responsive thermoreceptor⁹ exhibits altered subcellular localization and increased retrograde trafficking, thereby increasing the functional GCY-18 to GCY-23 ratio in the AFD sensory compartment. Altered GCY-23 localization and trafficking require PYT-1-dependent endocytosis, and we show that PYT-1-mediated modulation of the GCY-18 to GCY-23 protein ratio at the AFD sensory endings is necessary to shift the AFD response threshold toward warmer values following the temperature upshift. Our results describe a mechanism by which transcriptional and posttranscriptional mechanisms are temporally coordinated across sensory receptors to fine-tune experience-dependent plasticity in the response of a single sensory neuron type.

Whole-genome duplication (WGD) has had profound macroevolutionary impacts on diverse lineages,^1,2 preceding adaptive radiations in vertebrates,^3,4,5 teleost fish,^6,7 and angiosperms.^8,9,10 In contrast to the many known ancient WGDs in animals,^11,12 and especially plants,^13,14,15 we are aware of evidence for only four WGDs in fungi.^16,17 The oldest of these occurred ∼100 million years ago (mya) and is shared by ∼60 extant Saccharomycetales species,^18,19 including the baker's yeast Saccharomyces cerevisiae. Notably, this is the only known ancient WGD event in the yeast subphylum Saccharomycotina. The dearth of ancient WGD events in fungi remains a mystery.¹⁶ Some studies have suggested that fungal lineages that experience chromosome²⁰ and genome¹⁶ duplication quickly go extinct, leaving no trace in the genomic record, while others contend that the lack of known WGDs is due to an absence of data.^16,17 Under the second hypothesis, additional sampling and deeper sequencing of fungal genomes should lead to the discovery of more WGD events. Coupling hundreds of recently published genomes from nearly every described Saccharomycotina species, with three additional long-read assemblies, we discovered three novel WGD events. Although the functions of retained duplicate genes originating from these events are broad, they bear similarities to the well-known WGD that occurred in the Saccharomycetales.¹⁸ Our results suggest that WGD may be a more common evolutionary force in fungi than previously believed.

Vivid episodic memories in people have been characterized as the replay of multiple unique events in sequential order.^1,2,3,4 An important feature of this type of remembering is that we remember the identity of specific items and the contexts in which they occurred.^5,6,7,8,9 Animal studies demonstrate that rats remember multiple items and the contexts in which they occurred using episodic memory,¹⁰ and they replay the sequence of episodic memories.^11,12,13,14 However, whether rats remember the specific contexts in which event sequences occurred is not known. Here, we show that rats remember the flow of events and the contexts in which those events occurred. We trained rats to identify the third-to-last odor from lists presented in two distinct arenas using lists of trial-unique odors of unpredictable lengths. We first established that rats remember (1) ordinal information about two lists and (2) the encoding context of the lists. Next, we showed that rats simultaneously remember the order of events and the contexts in which they occurred. Finally, by interleaving contexts at unpredictable points in the lists, we demonstrated that rats replay episodic memories in a context-specific manner, with memory performance remaining robust even when the interleaving of lists was interrupted by a 30-min delay. These findings are consistent with the hypothesis that rats can replay streams of episodic memories within specific contexts. This capability suggests that rats may serve as a model for complex cognitive processes, which may ultimately provide insights into the biological mechanisms of memory, disorders of memory, and therapeutic interventions.

Leaf litter fall and processing in temperate streams is one of the most pervasive resource subsidies and ecosystem functions globally.^1,2,3 These subsidies are highly seasonally structured, yet their phenologies are shifting with climate change due to alterations of leaf senescence with global warming.^4,5,6 As phenology and phenological changes are species specific,⁷ the order of senescence of different leaf species is shifting.⁸ While the effect of phenology on community assembly and species interactions is well known, its influence on ecosystem function (particularly through the resource subsidy order of arrival and the duration between arrivals of different subsidies) remains underexplored.⁹ Here, we tested how the order of arrival and exposition duration of resource subsidies affect ecosystem function. We conducted a mesocosm experiment manipulating the order of arrival of two contrasting leaf species (high- and low-nutrient content), testing the effects of subsidy order and duration on decomposition rates by an abundant aquatic shredder. Exposure duration and arrival order of leaf species strongly influenced combined leaf litter consumption. Earlier arrival of high-quality leaves enhanced feeding on low-quality leaves. Shifting leaf fall duration and order of arrival thus has the potential to impact carbon cycling, even when the combined resource quantity remains constant. Our study demonstrates that these changes can have direct consequences on ecosystem processes in the context of the globally important function of leaf litter processing, emphasizing the need for incorporating temporal ecological aspects to understand the climate change impacts on the functioning of ecosystems.¹⁰.

Neoselachians (a monophyletic group including modern sharks, rays, and skates and their extinct relatives)^1,2 have an extensive fossil record and a long evolutionary history,^1,2,3 with over 1,100 extant species today.⁴ Previous reconstructions of their evolutionary history suggest a diversity peak in the Cretaceous, a severe decline across the Cretaceous-Paleogene (K/Pg),^5,6,7,8,9 and a prolonged stability thereafter,^7,8 aside from a small decline in the Pliocene.¹⁰ However, our knowledge of past neoselachian diversity has been mostly based on high taxonomic levels (e.g., genera or families),⁸ or from studies restricted to particular regions,^11,12,13 time periods,^5,9 or shark orders.^14,15 This is further complicated by spatiotemporal biases,^16,17 which can lead to apparent diversity changes, even when bias-correction methods are employed.^16,17 Using an extensive dataset of fossil occurrences¹⁸ and a deep-learning model that explicitly accounts for spatiotemporal and taxonomic sampling variation,¹⁹ we reconstruct the neoselachian diversity trajectory over the past 145 million years. We found a long-term increase during the Cretaceous, in which neoselachians reached modern diversity levels. Throughout the K/Pg, we recovered only a small (10%) decline, suggesting high turnover rather than a major extinction. Diversity then surged, culminating in a mid-Eocene peak, when neoselachians reached maximum richness. This peak was followed by a fluctuating yet downward trajectory toward the present, which overall resulted in a 41% loss of species and left modern diversity depleted compared to their thriving past. Together, our results reveal patterns hitherto obscured by multiple biases, challenging previous paradigms about neoselachian diversity.