Zoological Research最新文献

Brucellosis, a zoonotic disease caused by Brucella infection, poses a major threat to both global health and livestock productivity. Although reproductive impairment is well established, the molecular mechanisms driving testicular immunopathology remain poorly understood. In this study, single-cell RNA sequencing was used to delineate transcriptional changes in goat testicular tissues under physiological and Brucella-infected conditions, revealing dynamic immunological remodeling of the testicular microenvironment. Infection induced marked shifts in T cell and macrophage phenotypes, with T cells exhibiting pronounced hyperactivation linked to CD45-mediated signaling cascades. Thioredoxin-interacting protein ( TXNIP), a gene strongly up-regulated in response to infection, emerged as a potential immunotherapeutic target. Intercellular communication networks were significantly disrupted in infected testes, with CD39- and JAM-dependent signaling pathways implicated in the erosion of immune privilege. Regulon analysis further identified GATA3, IRF5, SEMA4A, and HCLS1 as transcriptional regulators associated with T cells and macrophages in infected testes. These findings provide novel insights into the molecular mechanisms driving testicular immunopathology during Brucella infection and highlight candidate targets for immunomodulatory intervention in disease control and livestock reproductive health.

Using comprehensive records from the World Spider Catalog, this study presents an in-depth, data-driven analysis of global trends in spider taxonomy, revealing an exceptional acceleration during the first quarter of the 21 ^st century. Of the more than 53 000 extant spider species described since 1757, 19 159-approximately 36%-were described during the last 25 years. In 59 families, the number of new species described during this period exceeded the total accumulated over the entire 20 ^th century. Asia emerged as the leading continental hotspot for spider discovery, with China at the forefront. The number of species described in China during the 25-year window was 1.5 times greater than the combined total documented over the preceding 243 years, with Chinese arachnologists responsible for 23.9% of all new species described in the last 25 years. Three taxonomists-Eugène Simon, Norman Platnick, and Shu-Qiang Li-rank as the most prolific contributors to spider systematics in history. These findings reflect a shift in the global center of arachnological research and underscore the growing scientific output from China. Patterns were examined from three complementary angles: temporal acceleration in species descriptions, individual contributions of leading taxonomists, and the emergence of Chinese arachnology as a dominant force in global taxonomy. Our analysis also emphasizes the critical role of sustained international collaboration in advancing biodiversity discovery.

Sex-biased dispersal, a widespread phenomenon in the animal kingdom, plays a crucial role in shaping genetic structure, optimizing population dynamics, and sustaining reproductive success. Recent research has uncovered considerable diversity and complexity in sex-biased dispersal patterns across species, although studies on snakes with secretive behaviors and low encounter rates remain limited. In this study, sex-biased dispersal in the Asian pitviper ( Viridovipera stejnegeri) was investigated using microsatellite markers and a mark-recapture approach. The underlying factors contributing to sex-biased dispersal were also examined, with a focus on genetic structure, kinship patterns, and resource competition. Microsatellite analyses revealed an overall pattern of female-biased dispersal in V. stejnegeri, although certain populations exhibited male-biased dispersal. Notably, these variations in dispersal patterns among populations were not associated with genetic differentiation. The contrasting results between microsatellite data and mark-recapture methods highlighted the limitations of using mark-recapture alone to investigate sex-biased dispersal in snakes. Analyses indicated no significant differences in intrasexual and intersexual resource competition pressures, thus failing to support the resource competition hypothesis. Kinship analysis showed no significant clustering of consanguineous individuals within subpopulations; rather, individuals dispersed into neighboring subpopulations through sex-biased dispersal, effectively reducing the risk of inbreeding and supporting the inbreeding avoidance hypothesis. However, further investigation is needed to determine whether the local mate competition hypothesis applies. Overall, this study provides valuable insights into methodological approaches and data interpretation relevant to biodiversity conservation and management strategies.

The sublaterodorsal tegmental nucleus (SLD) is a critical hub for regulating rapid eye movement (REM) sleep and muscle atonia, with its dysfunction linked to various disorders such as REM sleep behavior disorder (RBD) and cataplexy. Despite its physiological significance, the presynaptic patterns influencing SLD γ-aminobutyric acid (GABA)ergic neurons-one of the primary neuronal subtypes within the SLD-remain poorly understood. This study applied a modified rabies virus tracing system combined with a Cre/loxP-based genetic approach to map and quantify the whole-brain monosynaptic afferents to SLD GABAergic neurons in mice. In total, 139 anatomically distinct nuclei were identified as sources of direct input, with predominant projections originating from the midbrain, pons, and medulla. Ipsilateral contributions accounted for 67.99% of all traced inputs, while 32.01% were contralateral. Prominent sources included the mesencephalic reticular nucleus, superior colliculus, oral part of the pontine reticular nucleus, gigantocellular reticular nucleus, lateral hypothalamic area, and zona incerta neurons. Several nuclei displayed contralateral projection biases. Immunofluorescence staining revealed molecular diversity among input neurons, suggesting that SLD GABAergic neurons integrate signals from anatomically and functionally distinct neuronal populations. These findings provide a comprehensive anatomical framework for understanding how SLD GABAergic neurons integrate multisource inputs and offer new perspectives for investigating their involvement in regulating complex physiological functions, including sleep and motor control.

Enteritis, involving inflammation of the small intestine, is often accompanied by immune cell dysfunction during intestinal infections. Immunomodulatory β-glucans (BGs) have recently been shown to support antibacterial immune responses through the induction of trained immunity. However, little is known about the potential role of BG pretreatment in protecting against infectious enteritis in teleost fish. In this work, by establishing an adult zebrafish enteritis model via infection with the fish pathogen Edwardsiella piscicida and pretreating it with BGs, we demonstrated that such pretreatment confers protection against infectious enteritis, accompanied by reduced production of proinflammatory cytokines. Specifically, we found that BG pretreatment could amplify intestinal lectin pathway-associated complement activation to ameliorate the infectious enteritis. Moreover, through comprehensive RNA-seq analysis of immune cell marker genes in zebrafish, we revealed that the lectin pathway amplification by BG pretreatment modulated the responsiveness of intestinal Th17 cells, which was essential for the protection against infectious enteritis. Collectively, these findings identify the intestinal lectin pathway as a potential mediator of the effects of BG pretreatment and reveal its role in maintaining the function of Th17 cells in zebrafish. This suggests that harnessing BG-induced trained immunity might represent a promising therapeutic strategy against infectious enteritis in teleost.

Neuronal intranuclear inclusion disease (NIID) is a rare autosomal dominant neurodegenerative disorder defined by the presence of eosinophilic intranuclear inclusions across both central and peripheral components of the nervous system, as well as multiple visceral organs, resulting in pronounced clinical heterogeneity. Following the discovery of pathogenic GGC repeat expansions in the NOTCH2NLC gene as the underlying genetic driver, a diverse array of experimental platforms has been established to probe NIID pathogenesis, including adeno-associated virus-mediated expression systems, transgenic animal models, and patient-derived cellular systems such as brain organoids. Collectively, these models recapitulate key histopathological and behavioral phenotypes observed in NIID and have elucidated multiple molecular and cellular pathways implicated in disease progression. This review systematically examines the current landscape of NIID model systems, highlighting their respective contributions to understanding disease pathogenesis, evaluating their experimental limitations, and identifying avenues for future refinement. Such integrative analysis is critical for advancing the development of more faithful disease models and facilitating the identification of therapeutic targets for NIID.

Eggs represent an accessible and nutrient-dense source of high-quality animal protein, and decades of selective breeding have markedly elevated reproductive output in commercial laying hens. However, sustaining elevated productivity while improving eggshell integrity presents a critical challenge, as the molecular mechanisms of eggshell strength remain unclear. In this study, phenotypic assessment of eggshell strength was combined with single-cell transcriptomic profiling of the uterus from high- and low-strength groups, transcriptomic analysis of multiple tissues, and quantitative proteomic analysis of uterine fluid. Serum calcium and phosphorus levels did not differ significantly between groups. A single-cell atlas of the Rhode Island Red uterus was successfully generated for the first time, identifying nine distinct cell populations encompassing smooth muscle, epithelial, endothelial, and immune subsets. Integration of transcriptomic and proteomic datasets revealed that genes encoding collagens ( COL4A1/ 2, COL1A1/ 2, COL5A1, and COL6A1/ 2/ 3), solute carriers ( SLC4A4/ 7, SLC6A4, SLC9A2/ 9, and SLC38A2), ATPases ( ATP1A1, ATP1B1, ATP2B1/ 2, ATP2A2/ 3, and ATP2C1), calcium voltage-gated channels ( CACNB2, CACNA1C, and CACNA2D1), annexins ( ANXA5 and ANXA6), and integrins ( ITGB1 and ITGA9) were key molecular determinants associated with variation in eggshell strength. These genes were primarily enriched in signaling cascades involved in focal adhesion, actin cytoskeleton regulation, extracellular matrix (ECM)-receptor interactions, and calcium signaling. Notably, collagen family genes were predominantly localized to smooth muscle cells, consistent with the tissue remodeling and uterine inversion that occur during shell calcification, which may enhance spatial proximity between calcium ions and matrix proteins. These findings establish a multi-omics framework for understanding the uterine regulatory mechanisms underlying eggshell formation and offer a molecular foundation for breeding strategies aimed at prolonging laying cycles while preserving shell quality.

Oral ulcers (OUs) are among the most common lesions of the oral mucosa, typically associated with pain and burning sensations, and remain clinically challenging due to the scarcity of effective treatment options. Cy _RL-QN15, a novel ultra-short cyclic heptapeptide recently shown to promote skin repair, diabetic wound healing, and follicle neogenesis, was evaluated for its therapeutic potential in mucosal repair. Using a rat OU model and a primary oral epithelial cell inflammation model, Cy _RL-QN15 significantly accelerated wound closure through coordinated modulation of immune-epithelial crosstalk, including suppression of inflammatory cytokine release from macrophages and neutrophils, reduction of pro-inflammatory factor secretion by oral epithelial cells, and enhancement of their proliferation and migration. Mechanistic studies employing alanine scanning mutagenesis and microscale thermophoresis revealed that Cy _RL-QN15 directly interacted with Toll-like receptor 4 (TLR4) via a methionine-dependent binding interface (K _d=2.64 µmol/L), thereby inhibiting downstream MyD88/NF-κB signaling. As the first ultra-short cyclic heptapeptide identified to antagonize TLR4, Cy _RL-QN15 represents a mechanistically distinct immunomodulatory scaffold that restores mucosal homeostasis and offers a promising therapeutic candidate for TLR4-based OU intervention.

Ongoing climate change is driving high-altitude bird species to occupy even higher elevations, yet physiological and regulatory responses enabling these transitions remain poorly understood. This study investigated acute hypoxic responses in saker falcons ( Falco cherrug) inhabiting the Qinghai-Xizang Plateau by exposing individuals to simulated altitudes of 5 000-6 000 m above sea level (a.s.l.), exceeding their typical elevation range (approximately 4 300 m a.s.l.). GPS tracking data indicated that juvenile falcons maintained comparable activity levels across 4 000-5 000 m and 5 000-6 000 m a.s.l. ranges. However, pre-fledging individuals subjected to 6 000 m hypoxia for three days exhibited marked increases in hemoglobin concentration and blood glucose. Transcriptomic profiling revealed significant suppression of glycolytic activity, notably characterized by reduced expression of hexokinase 1 ( HK1), a key enzymatic gene involved in the glycolytic pathway. ATAC-seq further identified enhanced chromatin accessibility within the HK1 locus under hypoxia, revealing two conserved cis-regulatory elements recognized by the transcription factor NR3C1 in the hypoxia-treated group. NR3C1 expression was negatively correlated with HK1. Notably, both elements were unique and evolutionarily conserved in avian taxa, suggesting a potential role in hypoxia resilience among highland birds. These findings provide mechanistic insights into the molecular and physiological strategies employed by sakers to tolerate acute hypoxic stress and inform conservation efforts for high-altitude bird species on the Qinghai-Xizang Plateau and other alpine ecosystems facing accelerating climate change.

Oxidative stress arises from disruption of the balance between reactive oxygen species (ROS) production and detoxification and constitutes a fundamental driver of diverse pathological diseases. Skin photoaging is a well-recognized example, primarily driven by chronic ultraviolet (UV) exposure and marked by progressive structural and functional deterioration. UV-induced ROS accelerate macromolecular degradation and impair epidermal and dermal barrier integrity, highlighting the urgent need for effective antioxidant interventions. Antioxidant peptides (AOPs), whether naturally occurring or synthetically engineered, have shown considerable potential in mitigating ROS-induced cellular damage. Amphibians, which possess highly permeable skin and are continuously challenged by fluctuating environmental conditions, represent a rich source of bioactive peptides with potent antioxidant properties. In particular, AOPs isolated from amphibian skin secretions demonstrate notable efficacy in ROS scavenging and mitigation of oxidative damage, offering promising candidates for anti-photoaging therapies. This review provides an integrated overview of ROS generation and signaling, the molecular mechanisms linking oxidative stress to skin photoaging, and the emerging biomedical potential of amphibian-derived AOPs. Deeper mechanistic insight into their structure and function is expected to accelerate the development of novel peptide-based interventions for photoaging and other oxidative stress-associated dermatological disorders.