Current Biology最新文献

From tiny mosses to giant redwoods, around 450,000 species of land plants show a huge variety of forms, yet all land plants develop from stem cells in proliferative meristems. What makes a meristem? Two new papers suggest that low auxin signalling holds the key.

Thorns are modified branches that have evolved independently multiple times as defenses against herbivores. We previously identified the TCP transcription factors THORN IDENTITY1 (TI1) and TI2 as key regulators of thorn development in Citrus; however, how these genes are regulated remains unclear. In this study, using comparative transcriptomics, we identified TI3, encoding a SHORT INTERNODES/STYLISH (SHI/STY) family transcription factor that is specifically expressed in thorns. We found that TI3 binds to a previously undefined CTAG core element in the promoters of TI1 and TI2, activating their expression to promote stem cell arrest in the thorn meristem. CRISPR-Cas9-mediated disruption of TI3 function converted thorns into branches. Conversely, the PEBP family protein CsCENTRORADIALIS (CsCEN) represses TI3 expression in the axillary meristem to maintain stem cell activity and promote branch development. Mutations in CsCEN resulted in branch-to-thorn conversions, whereas cscen ti3 double mutants exhibited the ti3 mutant phenotype, supporting the idea that CsCEN regulates TI3 expression. The thorn-specific expression pattern of TI3 homologs across three Rutaceae species suggests that TI3 might have a conserved role in thorn development. Thus, TI3 represents a new regulator of meristem identity, and manipulating its activity is a promising approach for breeding thornless cultivars.

Nervous systems rely on sensory feature maps, where the tuning of neighboring neurons for some ethologically relevant parameter varies systematically, to control behavior. Such maps can be organized topographically or based on some computational principle. However, it is unclear how the central organization of a sensory system corresponds to the functional logic of the motor system. This problem is exemplified by insect flight, where sub-millisecond modifications in wing-steering muscle activity are necessary for stability and maneuverability. Although the muscles that control wing motion are anatomically and functionally stratified into distinct motor modules, comparatively little is known about the architecture of the sensory circuits that regulate their precise firing times. Here, we leverage an existing electron microscopy volume of an adult female ventral nerve cord (VNC) of the fruit fly Drosophila melanogaster to reconstruct the complete population of afferents in the haltere-nature's only biological "gyroscope"-and their synaptic partners. We morphometrically classify these neurons into distinct subtypes and design split-GAL4 lines that help us determine the peripheral locations from which each subtype originates. We find that each subtype, rather than originating from the same anatomical location, comprises multiple regions on the haltere. We then trace the flow of rapid mechanosensory feedback from the peripheral haltere receptors to the central motor circuits that control wing kinematics. Our work demonstrates how a sensory system's connectivity patterns construct a neural map that may facilitate rapid processing by the motor system.

Homeotic mutations result in developmental abnormalities in which one body part is replaced by another. In flowering plants, ABC mutations result in transformations between petals, stamens, pistils, and sepals,¹ while in insects, HOX mutations replace antennae with legs and abdominal segments with those of the thorax.² Homeotic mutations can help to reveal the genetic architecture governing development while providing insights into the evolutionary origins of an organism's body plan. Here, we identify a gene whose loss of function transforms the dorsal surface of the unicellular ciliate, Tetrahymena thermophila, normally devoid of cortical organelles, into a mirror-image of the ventral surface, complete with supernumerary contractile vacuole pores (CVPs) and a secondary oral apparatus (OA) exhibiting reversed local left-right asymmetry.³ Through next-generation sequencing (NGS), we discovered that JANA encodes a polo kinase that forms a circumferential cortical gradient, with a high point on the left-dorsal side of the cell. In Tetrahymena, polarized JanA/polo kinase localization appears to act in concert with other spatially restricted cortical morphogens to repress organelle assembly around most of the cell circumference, leaving a narrow wedge (a single ciliary row) to participate in oral assembly prior to cell division. Our study reveals a novel role for polo kinases in breaking the radial symmetry observed in early-divergent ciliates.

How do different brains create unique visual experiences from identical sensory input? While neural representations vary across individuals, the fundamental architecture underlying these differences remains poorly understood. Here, we reveal that individual visual experience emerges from a high-dimensional neural geometry across the visual cortical hierarchy. Using spectral decomposition of fMRI responses during naturalistic movie viewing, we find that idiosyncratic neural patterns persist across multiple orders of magnitude of latent dimensions. Remarkably, each dimensional range encodes qualitatively distinct aspects of individual processing, and this multidimensional neural geometry predicts subsequent behavioral differences in memory recall, including variation in the concreteness versus abstractness of narrative descriptions. These fine-grained patterns of inter-individual variability cannot be reduced to those detected by conventional intersubject correlation measures. Our findings demonstrate that subjective visual experience arises from information integrated across an expansive multidimensional manifold. This geometric framework offers a powerful new lens for understanding how diverse brains construct unique perceptual worlds from shared experiences.

Soil detritivores represent a major portion of terrestrial biodiversity and biomass. Their feeding activity accelerates the turnover of organic matter and nutrients, thereby enhancing energy and material flows within soil food webs. Yet, global environmental changes are increasingly disrupting terrestrial ecosystems, threatening soil detritivores and their ecological functions. We hypothesize that global environmental changes will result in a decline in the feeding activity of soil detritivores. To test this, we conduct a global meta-analysis, synthesizing 650 observations from 55 studies. Our results show that global environmental changes reduce the feeding activity of soil detritivores by 47.8% on average. Among GECs, climate change (-59.8%), chemical pollution (-57.6%), fire (-49.1%), and land-use intensification (-34%) exert the most pronounced detrimental effects. For climate change, drought (-68.9%) suppresses the feeding activity of soil detritivores to a far greater extent than warming (-25.4%). Notably, insecticides (-98.9%), fungicides (-59.7%), and heavy metals (-59.5%) are particularly harmful within chemical pollutants. The negative effects of land-use intensification are predominantly driven by mineral fertilization (-45.6%), whereas grazing (-20.3%) and tillage (-11.8%) have minor effects. The magnitude of reductions in soil detritivore feeding activity is strongly regulated by ecosystem type, soil properties (soil organic carbon and pH), and detritivore species richness and abundance. These findings suggest that global environmental change-induced declines in soil detritivore feeding activity may further impair energy transfer within soil food webs, with far-reaching implications for key ecosystem functioning in a rapidly changing global environment.

The fungus Candida albicans commensally colonizes mucosal surfaces in healthy individuals but can cause both superficial mucosal and life-threatening disseminated infections. The balance between commensalism and pathogenicity is complex and depends on factors including host and fungal genetic background, the host environment, and fungal interactions with local microbes. The major interaction interface of C. albicans with the host is its multilayered cell wall, which is dynamic and highly responsive to the surrounding environment. Therefore, factors that influence the fungal cell wall will directly impact C. albicans-host interactions. Our work demonstrates that multiple physiologically relevant gastrointestinal bacteria influence fungal cell wall composition during co-culture with C. albicans, including as complex communities derived from the gut. Using Escherichia coli as a model, we show that bacterial-induced fungal cell wall remodeling occurs rapidly and is mediated by secreted bacterial metabolite(s). Fungal mutant analysis revealed that the high osmolarity glycerol (HOG) pathway, which is critical for responding to environmental stresses, has an important role in regulating this cell wall remodeling phenotype through the Sln1 histidine kinase. Importantly, bacterial-mediated fungal cell wall remodeling increases C. albicans resistance to the echinocandins, increases macrophage phagocytic rates, and decreases recognition by human immunoglobulin A (IgA). Overall, this work comprehensively characterizes an interaction between C. albicans and common gastrointestinal bacteria that has important implications for fungal biology and host interactions.

Lichen symbioses frequently include additional fungal associates beyond the canonical mycobiont (fungus) and photobiont (alga/cyanobacterium). Despite the prevalence and diversity of these lichen cohabitants, their geographic distribution and role within the lichen consortium remain poorly understood. Combining genomics, metagenomics, and advanced microscopy, we identified the black fungus Melanina gundecimermaniae as a constant cohabitant in the lichen Umbilicaria pustulata. We analyzed metagenomes from 149 individuals across 15 populations, spanning the Europe-wide range of U. pustulata. Additionally, we screened pooled metagenomes of U. pustulata and Umbilicaria phaea along five elevation gradients (Europe and North America). Genome mapping, using a near-complete reference genome of M. gundecimermaniae, revealed that the black fungus was present in 100% of the screened lichen metagenomes, with 0.85%-3.78% of reads mapping against the reference. Among all lichen-associated fungi, it was one of the most common. These findings indicate that the black fungus is widely distributed and associated with different lichen species, underscoring its potential ecological significance. Using fluorescence in situ hybridization coupled with confocal laser scanning microscopy, we confirmed the presence of M. gundecimermaniae within various structures of U. pustulata, including vegetative symbiotic propagules involved in dispersal. Elucidating its widespread occurrence across continents, consistent presence in U. pustulata, and ability to be dispersed together with the lichens' canonical partners, our findings suggest a potential interaction of M. gundecimermaniae that extends beyond incidental colonization. Our study contributes to the growing body of evidence that organismal complexity within lichens is a prevalent and largely unexplored dimension of the lichen symbiosis.

Neurodegeneration often starts by atrophy of the cable-like nerve fibers (axons) that wire nervous systems. Maintaining axons requires supply via motor-protein-driven transport along uninterrupted bundles of microtubules. Functional loss of motor proteins, but surprisingly also their hyperactivation, links to conditions of axonal atrophy; in both cases the underlying mechanisms are little understood. To bridge this important knowledge gap, we carried out systematic studies using 40 different genetic tools to manipulate 19 context-related genes in one standardized Drosophila primary neuron system. Starting with transport motors, we found that downregulation in at least three of them-dynein heavy chain, the kinesin family member 5 (KIF5) ortholog kinesin heavy chain (Khc), and KIF1A ortholog Unc-104-caused disintegration of axonal microtubule bundles, which we refer to as "microtubule-curling"; this damages the essential highways for life-sustaining axonal transport. To understand this phenomenon, we focused on Khc's various subfunctions. We found that abolishing Khc-mediated mitochondrial and lysosomal transport affects the homeostasis of reactive oxygen species (ROS), which in turn triggers microtubule-curling in fly and mouse neurons alike. Taking the opposite approach by using conditions where Khc is hyperactive, we observed comparable microtubule-curling, triggered by an ROS-independent mechanism likely involving excessive mechanical force generation. To assess wider relevance of our findings, we studied Unc-104, its binding partner KIF-binding protein (KIFBP), and human KIF5A. These studies suggest that functional loss and hyperactivation of other transport motors also cause ROS-dependent and -independent microtubule-curling, which could therefore represent two fundamental pathways that link transport motors to microtubule bundle decay and neurodegeneration.