Zoological Research最新文献

Gene loss represents a powerful driver of adaptive evolution. Cetaceans, which underwent a profound transition from terrestrial to fully aquatic life, provide an excellent model for investigating this process. Comparative genomic analysis of the cold-sensitive ion channel transient receptor potential ankyrin 1 ( TRPA1) revealed lineage-specific patterns of degeneration across cetaceans. In toothed whales, the ancestral lineage exhibited extensive exon loss within the TRPA1 locus, whereas baleen whales showed signatures consistent with markedly reduced or absent TRPA1 expression. These molecular alterations were inferred to disrupt or abolish TRPA1 protein function across cetaceans. Integration of these findings with established experimental evidence from human and murine TRPA1 studies supported several adaptive hypotheses for TRPA1 gene loss, including tolerance to abrupt thermal fluctuations, attenuation of nociceptive responses in aquatic environments, specialization of integumentary sensory systems, and the emergence of echolocation-associated sensory trade-offs in toothed whales. Collectively, these findings expand the gene loss repertoire of cetaceans and provide novel insights into the molecular underpinnings of secondary aquatic adaptation in mammals.

Antlers represent the only known example of complete annual organ regeneration in mammals. Despite this unique regenerative capacity, the genetic mechanisms driving antler origin and morphological diversification across Cervidae remain poorly understood. This study assembled six high-quality chromosome-level genomes of cervids spanning four distinct tribes, including the first genomic reference for the tufted deer ( Elaphodus cephalophus). Comparative analyses across the Cervidae lineage identified signatures of positive selection on gene networks governing stem cell differentiation and bone metabolism, with elevated expression of these genes detected in antler developmental and regenerative tissues. Tribe-specific selective pressures in Cervini and Odocoileini further revealed convergent evolution targeting core developmental pathways, notably the RAS/MAPK pathway, implicating these pathways in both the emergence and enhancement of antler traits. In contrast, relaxed selective constraints in the antlerless Chinese water deer ( Hydropotes inermis) revealed disruptions in gene modules associated with tumor suppression and skeletal homeostasis, suggesting a rewiring of regulatory homeostasis. These findings highlight how antler evolution reshaped physiological trade-offs, including reduced oncogenic susceptibility and enhanced tissue regeneration and cyclic bone remodeling. This study advances current understanding of antler evolution and diversification, while providing genomic resources for mammalian regenerative biology.

Body shape evolution in vertebrates frequently involves modifications in vertebral number or patterns of vertebral fusion, with distinct lineages displaying divergent trajectories. This study investigated the morphological and genetic basis of body shape variation between Hebao red carp (HB, Cyprinus carpio wuyuanensis) and Yellow River carp (YR, Cyprinus carpio haematopterus). Although both subspecies share an identical vertebral count (35), the compressed morphology of HB was attributable to skeletal anomalies, including vertebral shortening and fusion. Genome-wide association and population genetic analyses were performed on F1 and F2 hybrid cohorts to identify loci associated with this phenotype. A total of 231 selective sweep regions were detected across chromosomes A06, A08, A16, B05, and B06, with a prominent locus on chromosome A08 (15.99-16.39 Mb) strongly correlated with body shape traits. Transcriptomic analysis revealed haplotype-dependent expression of rflna within this interval, implicating rflna in axial skeletal patterning. Functional validation using CRISPR/Cas9-mediated knockout of rfln in zebrafish ( Danio rerio) induced vertebral malformations, including axial shortening, kyphosis, fusion, and a rounded abdominal profile. These results delineate the morphological and molecular framework governing axial remodeling in HB and highlight a conserved regulatory role for rflna in teleost skeletal development.

Jumping has independently emerged as an effective escape strategy across multiple beetle lineages (order Coleoptera). Characterization of jumping behavior not only informs the development of bioinspired robotic systems but also advances understanding of adaptive processes and convergent evolution. However, despite extensive behavioral studies in beetles, the genetic mechanisms and evolutionary trajectories underlying this locomotor strategy remain largely unresolved. To elucidate the molecular basis of jumping adaptation and convergent evolution, a comparative genomic analysis was conducted using high-quality assemblies, including one newly generated genome, from jumping beetles representing three families and their non-jumping sister taxa spanning over 200 million years of evolutionary divergence. Genes associated with energy metabolism exhibited extensive signals of rapid evolution and positive selection in jumping beetles, consistent with the elevated energy requirements of explosive locomotion. These observations parallel previous reports linking energy metabolism genes to other high-demand locomotor modes such as flight, suggesting shared molecular signatures across functionally distinct behaviors. Jumping beetles exhibited convergent amino acid substitutions in bab1, a regulator of leg disc development, alongside evidence of positive selection and accelerated evolution in the dynein gene Dnai4 and a significant expansion in copy number of the skeletal muscle gene Fhl2. Together, these results implicate both limb morphogenesis and muscle performance genes in the emergence of beetle jumping. This study highlights key genetic mechanisms underlying behavioral innovation and offers novel insights into adaptive convergence in insect locomotion.

Bats represent a remarkable mammalian lineage, distinguished by the evolution of powered flight, sophisticated echolocation, exceptional longevity, and robust resistance to viral infections. These adaptations have contributed to their rapid and extensive diversification over a short evolutionary period. Extensive research on bat biology has elucidated key aspects of species diversity, adaptive evolution, and the molecular frameworks that confer resistance to viral pathogens. Recent integration of high-resolution multi-omics, single-cell transcriptomics, and advanced three-dimensional culture systems has significantly expanded exploration of bat biology at the molecular and cellular levels. This review consolidates current advances in our understanding of bat species diversification, development, and immunological adaptations with relevance to human health. Emphasis is placed on emerging technologies and methodologies that have transformed the study of bat physiology and host-pathogen interactions. Prospective avenues for research are also outlined, including the development of new animal models and the application of cutting-edge biotechniques. These advances are anticipated to expand the utility of bats as a critical platform for biomedical and evolutionary insight.

Arrhythmogenic cardiomyopathy (ACM) confers elevated risk of ventricular arrhythmias and sudden cardiac death, yet limitations in early lesion sampling and model development continue to hinder mechanistic and translational research. Clinical, pathological, and mutational profiles were examined in 24 individuals with ACM harboring PKP2 variants. Among these, a patient carrying the c.1132C>T mutation exhibited the earliest onset and presented both structural cardiac abnormalities and major adverse cardiovascular events. To facilitate disease modeling, the c.1147C>T variant-a previously reported pathogenic substitution located proximal to position c.1132 in PKP2-was selected to enhance the feasibility of generating a porcine model. The BE3 gene editing system was used to induce C>T mutation. Two single guide RNAs targeting the PKP2 gene were designed (sgRNA1 for c.1132C>T and sgRNA2 for c.1147C>T), yielding editing efficiencies of 42.9% and 25.9%, respectively. SgRNA1 was used to generate PKP2 ^+/- porcine fetal fibroblasts. A total of 14 cloned piglets were produced, including 11 viable and three stillborn PKP2 ^+/- individuals. By 24 months of age, PKP2 ^+/- pigs developed premature ventricular contractions and right ventricular dilatation. Histological analysis revealed adipocyte infiltration within the right ventricular wall, and electron microscopy demonstrated reduced desmosomal length and electron density consistent with desmosomal dysfunction. Transcriptomic profiling showed high expression of genes associated with lipid catabolic processes. This study established the first PKP2 ^+/- porcine model of ACM using BE3-mediated base editing, providing a valuable platform for elucidating early pathogenic mechanisms and evaluating therapeutic interventions.

Traumatic brain injury (TBI) remains a major public health challenge worldwide, particularly among individuals under 45 years of age, resulting in profound physical disability, neuropsychiatric impairment, and socioeconomic burden. Existing therapeutic strategies offer limited efficacy, underscoring the urgent need for novel treatment modalities. This study evaluated the neuroprotective potential of OM-LV20, an amphibian-derived bioactive peptide, in a murine model of TBI. Intraperitoneal administration of OM-LV20 following controlled cortical impact significantly reduced brain water content and attenuated neurological and cognitive deficits. Histological analysis, TUNEL staining, and ultrastructural assessments revealed suppression of neuronal degeneration and mitigation of mitochondrial dysfunction. Transcriptomic profiling, together with RT-qPCR and western blot analyses, revealed modulation of the expression of apoptosis-related genes and proteins, indicating a robust anti-apoptotic effect mediated through mitochondrial pathways. Additionally, OM-LV20 exhibited efficient permeability across the blood-brain barrier. These findings indicate that OM-LV20 exerted strong neuroprotective activity through targeted suppression of mitochondria-centered neuronal apoptosis, supporting its potential utility in ameliorating neurological dysfunction post-TBI. The diverse mechanistic actions identified for OM-LV20 provide a novel therapeutic avenue with considerable promise for enhancing neurological recovery in individuals with TBI.

Epilepsy, a prevalent neurological disorder, is characterized by recurrent, self-sustained seizures resulting from abnormal neuronal hyperexcitability. Epilepsy encompasses a wide spectrum of etiologies, pathophysiological mechanisms, and treatment responses, resulting in considerable phenotypic heterogeneity. Over the past few decades, animal models, ranging from simple organisms to complex species, have played a pivotal role in elucidating the cellular, molecular, and circuit mechanisms underlying seizure generation and propagation, while also facilitating the development of antiseizure medication and other therapeutic interventions. This review first outlines the mechanistic basis of epilepsy and systematically summarizes existing seizure and epilepsy models across diverse taxa, including zebrafish, rodents, and non-human primates (NHPs), with a focus on model-specific features, translational relevance, and therapeutic utility. Despite substantial progress, limitations persist in recapitulating the full complexity of human epilepsy. Recent advances in genetic engineering, neuromodulation technology, and brain organoids are refining model fidelity and enhancing alignment with precision medicine approaches. Cross-species integration offers a promising avenue for bridging preclinical findings with clinical application, advancing mechanistic insight, and the development of targeted therapies.

To cope with seasonal changes in food availability, animals need to optimize their behaviors, including shifts in temporal activity patterns and spatial use in habitats. Most studies focused on the temporal activity pattern or habitat use in two-dimensional (2D) space. However, studies on the simultaneous changes in temporal activity patterns and habitat use in three-dimensional (3D) space are limited. In this study, we used the great evening bat ( Ia io) to investigate differences in the activity pattern and space use during the summer and autumn. We collected and analyzed the Global Positioning System (GPS) data and activity data obtained from accelerometers. The results showed that bats displayed seasonal variations in their movement patterns. Specifically, compared with summer, I. io individuals were found to extend their foraging duration and adopt a low-energy consumption pattern of activity in autumn. Furthermore, there was a notable increase in the vertical extent of the 3D habitat utilization range for these bats, although the 2D habitat size in autumn remained similar to that in summer. These changes manifested both temporally and spatially, potentially as a response to the reduced availability of insect resources from summer to autumn, and the arrival of migratory birds in autumn as an alternative food source. Our results suggest that I. io seasonally adjust their foraging strategies and spatial use from two to three dimensions. Our study provides important insights into the seasonal behaviour dynamics of bats during summer and autumn, which may contribute to understanding their ecological strategies and inform conservation efforts.

Bacterial sepsis frequently progresses to hypoglycemia, a metabolic condition strongly associated with increased mortality. In this study, large yellow croakers were injected with phosphate-buffered saline (PBS) to establish a control group (CG) or exposed to an equivalent dose of Pseudomonas plecoglossicida, after which infected fish were categorized into moribund group (MG) or survival group (SG). Results showed that hepatic glycogen was rapidly depleted across all infected croakers, but severe hypoglycemia emerged only in the MG group, with blood glucose reduced to 0.80 mmol/L. Infection produced substantial oxidative and redox disruption, including accumulation of lipid peroxides, depletion of reduced glutathione (GSH), and a decline in the NAD ⁺/NADH ratio, although these fluctuations were markedly attenuated in the SG group compared to the MG group. MG group exhibited widespread metabolic deterioration, characterized by reduced intermediates across glycolysis, the tricarboxylic acid (TCA) cycle, and oxidative phosphorylation, decreased glycerides and fatty acids, clear mitochondrial swelling with cristae loss, and strong suppression of G6pc transcription. SG group displayed a distinct metabolic reconfiguration involving altered abundance of 26 lipid species (18 increased and eight decreased) and 13 carbohydrates (nine increased and four decreased). The most pronounced fluctuations were observed in the glycogen-shunt products, maltose elevated 47.78-fold relative to the CG and 7 995-fold relative to the MG, and D-(+)-trehalose elevated by 964.08-fold and 1 106.38-fold, respectively. Functional analyses identified pptse6 (ACRRS2_13720), a type VI secretion system (T6SS) effector, as a key virulence gene in P. plecoglossicida, whose absence reduced bacterial virulence by 808-fold. Another competitive T6SS effector, TreS, contributed to maltose and D-(+)-trehalose synthesis, with its deletion lowering production of these metabolites by 7.75-fold and 6.75-fold, respectively. Overall, these findings demonstrated that P. plecoglossicida causes profound disruption of central energy metabolism in large yellow croakers and induces hypoglycemia, with activation of the glycogen shunt closely associated with survival.