Zoological Research最新文献

Red light therapy is a clinically validated, noninvasive approach for improving skin structure and stimulating collagen renewal. However, the molecular mechanisms by which light therapy reverses collagen-related skin degeneration remain unclear. Using a natural aging mouse model, this study investigated the effects of red light therapy on skin structure and regeneration. Unlike other wavelengths, red light rapidly increased dermal thickness and stimulated epidermal renewal by enhancing collagen synthesis in dermal fibroblasts and activating collagen/integrin-induced proliferation and differentiation of epidermal keratinocytes, resulting in significant improvements in skin morphology. Mechanistically, red light increased endogenous TGFβ expression in fibroblasts, which up-regulated type I collagen mRNA and protein expression via activation of SMAD2/3/4 nuclear translocation. Simultaneously, red light elevated intracellular cAMP, triggering AKT activation that inhibited matrix metalloproteinase expression via the NRF2/HO-1-dependent pathway, thereby reducing collagen degradation. The accumulation of type I collagen in dermal fibroblasts stimulated integrin signaling, promoting epidermal keratinocyte proliferation and differentiation. Red light-induced AKT activation also enhanced fibroblast proliferation, further amplifying collagen production and collagen-mediated epidermal renewal. These findings elucidate the mechanisms by which red light stimulates endogenous TGFβ and AKT signaling to regulate type I collagen production, driving coordinated dermis-epidermis remodeling. This pathway represents a potential therapeutic target for the prevention and treatment of age-related dermal degeneration.

Social hierarchies are central to the organizational structure of group-living species, shaping individual physiology, behavior, and social interactions. Dopaminergic (DA) systems, particularly within the ventral tegmental area (VTA) and dorsal raphe nucleus (DR), have been linked to motivation and competitive behaviors, yet their region-specific contributions to social dominance remain insufficiently defined. This study investigated the role of VTA and DR DA neurons in regulating social dominance in sexually naïve male C57BL/6J mice. Stable hierarchies were established using the tube test, after which both dominant and subordinate mice exhibited elevated c-Fos expression within the VTA and DR. Notably, dominant mice displayed significantly greater c-Fos activation in DR DA neurons compared to subordinates. Fiber photometry revealed that DA neurons in both regions were activated during proactive push behaviors and inhibited during passive retreats, with DR neurons showing stronger activation during dominance-related actions. Chemogenetic inhibition of DR DA neurons in dominant mice reduced their social rank, whereas activation in subordinates elevated their rank. In contrast, chemogenetic modulation of VTA DA neurons had no significant effect on social dominance. Manipulation of DA neurons in both regions produced rank-dependent changes in specific anxiety-like behavioral phenotypes. These findings highlight the distinct roles of DR and VTA DA neurons in social hierarchy regulation, identifying DR DA neurons as a critical component in the modulation of social dominance.

Male infertility constitutes a major global public health concern, with the underlying etiology remaining unidentified in nearly half of the diagnosed cases. Protein kinase CK1α (CK1α) functions as a pivotal regulator of cell cycle progression, pre-mRNA processing, and spliceosome-associated pathways through interactions with specific splicing factors. Comprehensive analyses revealed CK1α expression in both germ cells and somatic cells of mouse testes, implicating its involvement in spermatogenic regulation. However, the physiological roles and mechanistic basis of CK1α function in Sertoli cells remain unclear. In this study, CK1α was highly expressed in Sertoli cells, and conditional knockout of CK1α in murine Sertoli cells induced profound testicular atrophy and complete infertility. This phenotype was characterized by rapid depletion of Sertoli cells and spermatogenic dysfunction. Subsequent analyses demonstrated that CK1α regulated the fate determination of fetal and neonatal Sertoli cells in mice. At the molecular level, CK1α promoted Sertoli cell survival through interaction with the splicing factor ZRSR1 to modulate apoptosis. Collectively, these findings establish CK1α as a key regulator of alternative splicing and male reproduction, providing critical insights into the molecular mechanisms underlying testicular development and reproductive function.

Zona pellucida glycoprotein-1 (ZP1) is essential for maintaining oocyte structural integrity and facilitating fertilization. Mutations in ZP1 are strongly associated with primary infertility disorders such as fertilization failure and empty follicle syndrome; however, the absence of accurate experimental models has hindered mechanistic understanding and obscured the etiological basis of ZP1-related infertility. In this study, CRISPR/Cas9-mediated genome editing was employed to generate two ZP1-edited cynomolgus macaques ( Macaca fascicularis), designated #ZP1-1 (male) and #ZP1-2 (female). Following sexual maturation, oocytes retrieved from #ZP1-2 through superovulation exhibited a marked increase in zona pellucida-deficient oocytes and a significant reduction in maturation rates compared to controls. Integrated analyses, including immunofluorescence staining, transmission electron microscopy, transcriptomic profiling of oocytes, and histopathological examination of ovarian tissue, revealed disrupted folliculogenesis and oocyte anomalies consistent with phenotypes observed in human empty follicle syndrome. These findings establish the ZP1-knockout cynomolgus macaque as the first non-human primate model of ZP1-related infertility, providing a valuable platform for elucidating disease mechanisms and informing the development of targeted interventions for infertility arising from ZP gene mutations.

The big-headed turtle ( Platysternon megacephalum), currently the only extant member of the genus Platysternon and the family Platysternidae, has undergone severe population declines driven by poaching, illegal trade, and habitat loss, leading to its classification as Critically Endangered (CR) by the International Union for Conservation of Nature (IUCN). Despite its conservation status, persistent taxonomic ambiguities and unresolved phylogenetic relationships have hindered effective protection and management. This study integrated evidence from genome-wide single nucleotide polymorphisms (SNPs), mitochondrial DNA sequences ( COI, 12S), and morphological data to reconstruct the phylogeny and phylogeography of Platysternon and revise its taxonomy. Results revealed that Platysternon megacephalum megacephalum and Platysternon megacephalum peguense represent deeply divergent evolutionary lineages, which are herein recognized as distinct species, Platysternon megacephalum Gray, 1831 sensu stricto and Platysternon peguense Gray, 1870. The subspecies Platysternon megacephalum shiui Ernst & McCord, 1987 is taxonomically invalid. In addition, a highly divergent lineage endemic to the Baise-Hechi region of Guangxi is described as a third species, Platysternon baiseensis sp. nov. This revised taxonomic framework resolves key phylogenetic relationships and delineates species boundaries, establishing a robust systematic foundation for big-headed turtles and providing a critical taxonomic basis for future conservation efforts targeting this endangered group of turtles.

Effective countermeasures against multidrug-resistant nosocomial pathogens, such as carbapenem-resistant Klebsiella pneumoniae and methicillin-resistant Staphylococcus aureus (MRSA), require the development of innovative antimicrobial strategies. This study presents a structure-function approach to antimicrobial peptide (AMP) design through the strategic integration of a cationic backbone with a hydrophobic core. This dual-domain architecture enables robust hydrophobic and electrostatic interactions, promoting spontaneous self-assembly and efficient membrane engagement. The lead peptide, Tryptolycin (TRPY), formed stable, monodisperse nanoparticles and demonstrated broad-spectrum bactericidal activity, with minimum inhibitory concentrations ≤1 µmol/L against multiple strains of MRSA and K. pneumoniae, while exerting minimal cytotoxicity toward mammalian cells. TRPY achieved rapid bacterial elimination, eradicating 99.9% of both planktonic and persister populations within minutes. Mechanistic investigations revealed that TRPY induced membrane permeabilization, promoted reactive oxygen species (ROS) production, and inhibited biofilm formation. In murine infection models, TRPY effectively eradicated established infections, reducing bacterial burden across target organs by 3- to 5-fold without significant cytotoxicity at therapeutic concentrations. Collectively, these findings establish TRPY as a promising therapeutic agent for clinical translation in the treatment of refractory bacterial infections.

Liver-expressed antimicrobial peptide 2 (LEAP2) is a key regulator of innate immune defense in teleosts, yet the molecular basis of its chemotactic function remains largely unidentified. Boleophthalmus pectinirostris MOSPD2 ( BpMOSPD2) was previously identified as a candidate receptor for BpLEAP2 in monocytes/macrophages (MO/MΦ). In the present study, BpLEAP2 stimulation was found to trigger a retromer-dependent intracellular trafficking program essential for BpMOSPD2-mediated chemotaxis. Exposure to BpLEAP2 significantly enhanced BpMO/MΦ migration and promoted the accumulation of BpMOSPD2 at the plasma membrane. Subcellular fractionation and immunofluorescence analyses revealed that BpMOSPD2 translocated from the endoplasmic reticulum (ER) to early endosomes upon BpLEAP2 stimulation, followed by redistribution to the cell surface. Blockade of ER export or knockdown of core retromer subunits ( BpVPS35, BpVPS26, or BpVPS29) abolished membrane localization and attenuated BpLEAP2-induced migration. Co-immunoprecipitation combined with mass spectrometry confirmed direct binding between BpMOSPD2 and BpVPS35, while domain-mapping indicated that this interaction was not exclusively dependent on MSP or CRAL-TRIO domains. Depletion of individual retromer components led to retention of BpMOSPD2 in early endosomes, establishing the necessity of the retromer complex for receptor recycling. Functionally, disruption of this complex eliminated the pro-migratory activity of BpLEAP2 on BpMO/MΦ. These findings identify the retromer complex as a critical regulator of BpMOSPD2 trafficking and uncover a previously unrecognized mechanism through which BpLEAP2 promotes MO/MΦ migration in teleosts.

Estrus represents a critical phase in the porcine reproductive cycle and relies on functional ovarian development and coordinated steroidogenesis. Granulosa cells (GCs) mediate these processes by secreting estradiol (E ₂) and progesterone (P ₄), which are essential for follicular maturation and ovulatory competence. While circular RNAs (circRNAs) have been implicated in steroid hormone synthesis, their involvement in the regulation of gilt estrous remains unclear. In this study, circRNA sequencing was performed on ovarian tissues of estrus (ES) and non-estrus (NES) gilts, resulting in the identification of a novel circRNA, termed circular SHOC2 leucine rich repeat scaffold protein (circSHOC2), which exhibited marked up-regulation in ES ovaries. Functional assays demonstrated that circSHOC2 overexpression enhanced E ₂ and P ₄ synthesis and increased the protein levels of key steroidogenic enzymes. Mechanistic investigation revealed that circSHOC2 sponges miR-130b-5p. Silencing miR-130b-5p significantly enhanced E ₂ and P ₄ production, along with the up-regulation of steroidogenic proteins. Additionally, miR-130b-5p targeted ASH1-like histone lysine methyltransferase (ASH1L), while its overexpression significantly inhibited ASH1L. Cotransfection experiments revealed that ASH1L mitigated the inhibitory effects of miR-130b-5p on E ₂ and P ₄ synthesis in GCs. These findings establish a regulatory axis in which circSHOC2 modulates steroidogenic capacity in porcine GCs via the miR-130b-5p/ASH1L pathway, offering mechanistic insight into the molecular basis of gilt estrus and providing potential targets to enhance reproductive efficiency.

Life-history traits represent evolutionary adaptations that mediate responses to external environments. Analyzing variation in these traits provides valuable insights into macroecological processes and supports the development of effective conservation and restoration strategies. However, large-scale biogeographic patterns in life-history trait diversity among terrestrial vertebrates remain insufficiently characterized, and the processes shaping these patterns are not well understood. This study integrated life-history and spatial distribution data for 2 334 terrestrial vertebrate species in China, including 398 amphibians, 211 reptiles, 541 mammals, and 1 184 birds, to evaluate spatial patterns of trait diversity and identify underlying drivers. Assemblages in South and Southwest China exhibited high species richness, substantial assemblage-level evolutionary distinctiveness, expanded trait volumes, and elevated trait densities compared to null expectations, indicating roles as both evolutionary museums and cradles. In contrast, assemblages on the Tibetan Plateau showed expanded trait volumes but low trait densities, reflecting niche expansion among limited taxa. These findings emphasize the importance of niche packing before assemblages reach environmental carrying limits. Assemblages with high evolutionary distinctiveness tended to display high trait volumes and low trait densities, suggesting a consistent relationship between phylogenetic structure and functional diversification. Among the four groups, amphibians showed the highest sensitivity to environmental variation, highlighting the need for focused conservation efforts. Overall, this study revealed pronounced spatial heterogeneity in trait diversity across China, shaped by species richness, evolutionary distinctiveness, and environmental variation, providing valuable insights for refining conservation priorities for terrestrial vertebrate taxa.

Intestinal inflammation is a common challenge in intensive aquaculture, yet its pathogenesis remains unclear. While interleukin 22 (IL-22) is recognized as a critical regulator of cellular homeostasis during inflammation in higher vertebrates, its roles in fish are not well understood. This study established hypoxia-induced models in intestinal tissues and primary intestinal epithelial cells of yellow catfish to investigate the involvement of IL-22 in maintaining intestinal homeostasis. Results revealed that Pelteobagrus fulvidraco IL-22 ( Pf_ IL-22) was abundantly expressed in mucosal tissues, with the highest levels in the gill and intestine. Hypoxia induced pronounced intestinal injury, characterized by loosening of the lamina propria and extensive vacuolization, while activating hypoxia-inducible factor (HIF) signaling and markedly up-regulating IL-22 expression. IL-22 levels peaked at 24 h post-hypoxia, suggesting a role in early immune responses. Recombinant Pf_IL-22 also induced transcription of pro-inflammatory mediators, including IL-1β and tumor necrosis factor α (TNF-α), in primary intestinal epithelial cells, indicating a dual regulatory function in balancing protection and inflammation. Mechanistic analyses revealed that HIF-1α directly interacted with a hypoxia response element within the IL-22 promoter to drive transcription, as confirmed by dual-luciferase assays, electrophoretic mobility-shift assays, and HIF-1α knockdown. Silencing Pf_IL-22 significantly suppressed Th17 cell differentiation pathways, demonstrating its role in shaping downstream immune responses. These findings establish the HIF-1α/IL-22 axis as a key regulatory pathway modulating immune responses and alleviating intestinal inflammation, providing a basis for developing IL-22-targeted immunotherapies and selective breeding strategies in aquaculture.