Zoological Research最新文献

The family Hepeviridae has seen an explosive expansion in its host range in recent years, yet the evolutionary trajectory of this zoonotic pathogen remains largely unknown. The emergence of rat hepatitis E virus (HEV) has introduced a new public health threat due to its potential for zoonotic transmission. This study investigated 2 464 wild small mammals spanning four animal orders, eight families, 21 genera, and 37 species in Yunnan Province, China. Using broadly reactive reverse transcription-polymerase chain reaction (RT-PCR), we systematically screened the presence and prevalence of Orthohepevirus and identified 192 positive specimens from 10 species, corresponding to an overall detection rate of 7.79%. Next-generation sequencing enabled the recovery of 24 full-length genomic sequences from eight host species, including Bandicota bengalensis, Eothenomys eleusis, and Episoriculus caudatus, representing newly reported host species for Orthohepevirus strains. Phylogenetic and sequence analyses revealed extensive genetic diversity within orthohepeviruses infecting rodents and shrews. Notably, among the identified strains, 20 were classified as Rocahepevirus ratti C1, two as C3, and one as Rocahepevirus eothenomi, while the remaining strain exhibited significant divergence, precluding classification. Evolutionary analyses highlighted close associations between orthohepeviruses and their respective host taxa, with distinct phylogenetic clustering patterns observed across different host orders. These findings emphasize the critical roles of co-speciation and cross-species transmission in shaping the evolutionary trajectories of the genera Paslahepevirus and Rocahepevirus.

Iron is the most abundant transition metal in the brain and is essential for brain development and neuronal function; however, its abnormal accumulation is also implicated in various neurological disorders. The olfactory bulb (OB), an early target in neurodegenerative diseases, acts as a gateway for environmental toxins and contains diverse neuronal populations with distinct roles. This study explored the cell-specific vulnerability to iron in the OB using a mouse model of intranasal administration of ferric ammonium citrate (FAC). Olfactory function was assessed through olfactory discrimination tests, while iron levels in OB tissues, cerebrospinal fluid (CSF), and serum were quantified using inductively coupled plasma mass spectrometry (ICP-MS), immunohistochemical staining, and iron assays. Transcriptomic changes and immune responses were assessed using RNA sequencing and immune cell infiltration analysis. Results showed that intranasal FAC administration impaired olfactory function, accompanied by iron deposition in the olfactory mucosa and OB, as well as damage to olfactory sensory neurons. Notably, these effects occurred without elevations in CSF or serum iron levels. OB iron accumulation activated multiple immune cells, including microglia and astrocytes, but did not trigger ferroptosis. Spatial transcriptomic sequencing of healthy adult mouse OBs revealed significant cellular heterogeneity, with an abundance of neuroglia and neurons. Among neurons, GABAergic neurons were the most prevalent, followed by glutamatergic and dopaminergic neurons, while cholinergic and serotonergic neurons were sparsely distributed. Under iron-stressed conditions, oligodendrocytes, dopaminergic neurons, and glutamatergic neurons exhibited significant damage, while GABAergic neurons remained unaffected. These findings highlight the selective vulnerability of neuronal and glial populations to iron-induced stress, offering novel insights into the loss of specific cell types in the OB during iron dysregulation.

Severe combined immunodeficiency disease (SCID), characterized by profound immune system dysfunction, can lead to life-threatening infections and death. Animal models play a pivotal role in elucidating biological processes and advancing therapeutic strategies. Recent advances in gene-editing technologies, including zinc-finger nucleases (ZFNs), transcription activator-like effector nucleases (TALENs), CRISPR/Cas9, and base editing, have significantly enhanced the generation of SCID models. These models have not only deepened our understanding of disease pathophysiology but have also driven progress in cancer therapy, stem cell transplantation, organ transplantation, and infectious disease management. This review provides a comprehensive overview of current SCID models generated using novel gene-editing approaches, highlighting their potential applications in translational medicine and their role in advancing biomedical research.

Increasing evidence implicates disruptions in testicular fatty acid metabolism as a contributing factor in non-obstructive azoospermia (NOA), a severe form of male infertility. However, the precise mechanisms linking fatty acid metabolism to NOA pathogenesis have not yet been fully elucidated. Multi-omics analyses, including microarray analysis, single-cell RNA sequencing (scRNA-seq), and metabolomics, were utilized to investigate disruptions in fatty acid metabolism associated with NOA using data from public databases. Results identified ACSL6, ACSBG2, and OLAH as key genes linked to fatty acid metabolism dysregulation, suggesting their potential causative roles in NOA. A marked reduction in omega-3 polyunsaturated fatty acids, especially docosahexaenoic acid (DHA), was observed, potentially contributing to the pathological process of NOA. Sertoli cells in NOA patients exhibited apparent fatty acid metabolic dysfunction, with PPARG identified as a key transcription factor (TF) regulating this process. Functional analyses demonstrated that PPARG is crucial for maintaining blood-testis barrier (BTB) integrity and promoting spermatogenesis via regulation of fatty acid metabolism. These findings reveal the pivotal role of fatty acid metabolism in NOA and identify PPARG as a potential therapeutic target.

The CRISPR-Cas13 system, an RNA-guided editing tool, has emerged as a highly efficient and stable RNA editing technique. Although the CRISPR-Cas13 system has been developed in several insect species, its application in lepidopterans has not yet been reported. In the present study, we evaluated the RNA cleavage activity of the CRISPR-Cas13 system in the silkworm ( Bombyx mori), a model lepidopteran insect, both ex vivo and in vivo. We established two stable silkworm BmE cell lines expressing PspCas13b and CasRx, respectively. Further analysis demonstrated that both PspCas13b and CasRx effectively down-regulated the transcription of exogenously-introduced target and endogenous genes in these cell lines. In addition, we generated two transgenic silkworm strains, one expressing CasRx and the other expressing RNA-guided CRISPR RNA targeting Sex combs reduced ( Scr). Further crossing experiments showed that CasRx induced a down-regulation of Scr transcription in silkworms, which impaired systemic growth of larvae. Overall, this study demonstrated that the CRISPR-Cas13 RNA editing system works efficiently in the silkworm, providing a potential alternative approach for RNA manipulation in lepidopteran insects.

In group-living animals, chronic juvenile social isolation stress (SIS) can profoundly affect behavior and neuroendocrine regulation. However, its impact on social behavior in avian species, particularly regarding sex-specific neural circuit differences, remains underexplored. This study focused on zebra finches, a species known for its social clustering and cognitive abilities, to elucidate these influences. Results indicated that SIS significantly increased plasma corticosterone levels in females but not in males, suggesting a heightened stress response and susceptibility in females. Additionally, SIS disrupted sociality and flocking behavior in both sexes, with more severe impairments in social recognition observed in females. Mesotocin (MT) levels in the lateral septum of both sexes and in the ventromedial hypothalamus of females were found to mediate the SIS effect, while vasotocin (VT) levels within the social behavior network remained unchanged. Pharmacological interventions confirmed the critical role of MT in reversing SIS-induced impairments in sociality, flocking behavior, and social recognition, particularly in females. These findings highlight unique nucleus- and sex-dependent variations in MT and VT regulation, providing novel insights into the mechanisms governing avian social behavior. This study advances our understanding of the independent evolutionary pathways of neural circuits and neuroendocrine systems that modulate social behaviors across different taxonomic groups.

Animals deploy diverse color-based defenses against predators, including crypsis, mimicry, aposematism, and masquerade. While crypsis, mimicry, aposematism have been extensively studied, the strategy of masquerade-where organisms imitate inedible or inanimate objects such as leaves, twigs, stones, and bird droppings-remains comparatively underexplored, particularly in adult butterflies. The Indian oakleaf butterfly ( Kallima inachus) exemplifies this phenomenon, with its wings resembling dead leaves, providing a classic example of natural selection. Although it has long been postulated that these butterflies evade predation by being misidentified as dead leaves, direct experimental evidence is lacking. In the current study, using domestic chicks as predators, we manipulated their prior experience with dead leaves (model objects) while maintaining constant exposure to butterflies to test whether dead-leaf masquerade provides a protective advantage by preventing recognition. Results showed a marked delay in the initiation of attacks by chicks familiar with dead leaves compared to those with no prior exposure or those exposed to visually altered leaves. Chicks with prior dead-leaf experience required a similar amount of time to attack the butterflies as they did to attack dead leaves. These findings provide the first empirical demonstration of dead-leaf masquerade in Kallima butterflies, shedding light on its evolutionary significance. Our study highlights the effectiveness of masquerade in inducing the misclassification of butterflies as inanimate objects, showcasing the precise mimicry achieved by these organisms when viewed in isolation from the model objects. This study advances our understanding of the evolution of masquerade and its role as a potent antipredator strategy in nature.

Long non-coding RNAs (lncRNAs), which are RNA molecules longer than 200 nucleotides that do not encode proteins, are implicated in a variety of biological processes, including growth and development. Despite research into the role of lncRNAs in skeletal muscle development, the regulatory mechanisms governing ovine skeletal muscle development remain unclear. In this study, we analyzed the expression profiles of lncRNAs in skeletal muscle from 90-day-old embryos (F90), 1-month-old lambs (L30), and 3-year-old adult sheep (A3Y) using RNA sequencing. In total, 4 738 lncRNAs were identified, including 997 that were differentially expressed. Short-time series expression miner analysis identified eight significant expression profiles and a subset of lncRNAs potentially involved in muscle development. Kyoto Encyclopedia of Genes and Genomes enrichment analysis revealed that the predicted target genes of these lncRNAs were primarily enriched in pathways associated with muscle development, such as the cAMP and Wnt signaling pathways. Notably, the expression of lncRNA GTL2 was found to decrease during muscle development. Moreover, GTL2 was highly expressed during the differentiation of skeletal muscle satellite cells (SCs) and was shown to modulate ovine myogenesis by affecting the phosphorylation levels of PKA and CREB. Additionally, GTL2 was found to regulate both the proliferation and differentiation of SCs via the PKA-CREB signaling pathway. Overall, this study provides a valuable resource and offers novel insights into the functional roles and regulatory mechanisms of lncRNAs in ovine skeletal muscle growth and development.

Animal models constructed using pathogenic factors have significantly advanced drug development for Alzheimer's disease (AD). These predominantly transgenic models, mainly in mice, replicate pathological phenotypes through gene mutations associated with familial AD cases, thus serving as vital tools for assessing drug efficacy and for performing mechanistic studies. However, the species-specific differences and complex, heterogeneous nature of AD etiology pose considerable challenges for the translatability of these animal models, limiting their utility in drug development. This review offers a comprehensive analysis of widely employed rodent (mice and rats) and non-rodent models ( Danio rerio (zebrafish), Drosophila melanogaster, and Caenorhabditis elegans), detailing their phenotypic features and specific research applications. This review also examines the limitations inherent in these models and introduces various strategies for expanding AD modeling across diverse species, emphasizing recent advancement in non-human primates (NHPs) as valuable models. Furthermore, potential insights from the integration of innovative technologies in AD research are discussed, while providing valuable perspectives on the future development of AD animal models.

Previous research has highlighted the significant role of progestins and glucocorticoids in fish oocyte maturation and ovulation. To clarify the molecular mechanisms underlying these processes, comprehensive investigations were conducted using a cyp17a2 mutant Nile tilapia ( Oreochromis niloticus) model. Analysis revealed pronounced Cyp17a2 expression in ovarian somatic cells of the tilapia. Female cyp17a2-deficient mutants exhibited markedly reduced levels of 17,20β-dihydroxy-4-pregnen-3-one (DHP) and cortisol/cortisone, leading to delayed meiotic initiation and impaired oocyte maturation and spawning. Notably, supplementation with human chorionic gonadotrophin (hCG), DHP, and cortisol effectively induced germinal vesicle breakdown (GVBD) and facilitated oocyte release with follicular cell layers in cyp17a2 ^-/- females. Additionally, cyp17a2 ^-/- and rescued cyp17a2 ^-/- females showed elevated transcription of steroidogenic enzymes involved in 17β-estradiol (E2) production compared to spawning wild-type females. Moreover, the reduction in Akt phosphorylation observed in cyp17a2-deficient females and upon inhibitor treatment impaired hCG-induced oocyte maturation. Conversely, activation of the phosphoinositide 3-kinase/protein kinase B (PI3K-Akt) signaling pathway partially rescued the oocyte maturation impairment caused by cyp17a2 mutation. Overall, these findings provide functional evidence supporting the critical role of Cyp17a2 in DHP and cortisol biosynthesis, which, in turn, facilitates oocyte maturation and ovulation through activation of the PI3K-Akt signaling pathway in fish.