摘要: 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 na?ve 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 cFos 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 dominancerelated 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.

摘要: Bivalve mollusks represent a taxonomically and economically significant clade within Mollusca. However,the regulatory mechanisms governing their embryonic development remain poorly characterized. The dwarf surf clam(Mulinia lateralis), characterized by a short generation time and high fecundity, has recently gained recognition as an ideal model system for bivalve embryological research. This study explored the epigenetic mechanisms driving embryogenesis in M. lateralis, with a particular focus on the maternal-to-zygotic transition(MZT), by integrating chromatin-state profiling and transcriptomic analysis. For the first time in this species,CUT&Tag was employed to generate high-resolution landscapes of histone modifications H3K4me1, H3K4me3,H3K27me3, and H3K27ac across key developmental stages. The resulting data revealed extensive reprogramming of histone marks, indicating dynamic shifts in chromatin architecture during early embryonic development. Integration with transcriptomic data identified the timing of MZT in M. lateralis between the morula and gastrula stages and highlighted a suite of candidate genes essential for embryogenesis. These findings provide mechanistic insight into chromatin-mediated control of bivalve embryogenesis and establish M. lateralis as a robust platform for epigenomic research in marine invertebrates, with implications for functional gene studies and aquaculture advancement.

摘要: Apoptosis preserves organismal homeostasis by selectively eliminating unnecessary or damaged cells, with accumulating evidence also suggesting that it activates regenerative pathways and facilitates tissue remodeling.To date, however, the regulatory mechanisms linking this form of programmed cell death to regeneration remain poorly defined, particularly in evolutionarily basal organisms. Using the sea cucumber（Apostichopus japonicus） as a model for intestinal regeneration, this study identified robust apoptotic activity across key regenerative stages. Pharmacological suppression of apoptosis during wound healing and mesenteric scaffold formation critically impaired intestinal regeneration. Quantitative proteomics using direct data-independent acquisition（DIA） revealed coordinated down-regulation of lipid metabolic pathways under apoptosis-inhibited conditions, with notable suppression of Ca²⁺ -independent phospholipase A2（i PLA2）, an enzyme typically up-regulated during successful regeneration. In parallel, expression of regeneration-associated factors WNT6 and EGFL7 was markedly reduced under apoptotic blockade. Targeted inhibition of iPLA2, EGFL7, or WNT6 each resulted in impaired mesenteric outgrowth and reduced proliferative activity within the regenerating intestinal primordia.Collectively, these findings suggest two potential mechanistic pathways: apoptosis-mediated regeneration of lipid metabolism via iPLA2 and apoptosis-dependent activation of WNT6/EGFL7 signaling. This study provides mechanistic insight into apoptosis-coupled regenerative processes in basal deuterostomes and expands the conceptual framework of programmed cell death in tissue renewal.

摘要: 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, 1831sensu stricto and Platysternon peguense Gray, 1870. The subspecies Platysternon megacephalum shiui Ernst &Mc Cord, 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.

摘要: The collision of the Indian and Eurasian plates during the Eocene represents a major tectonic shift that significantly altered biotic dynamics and promoted species diversification across the Oriental region. To explain the diversification of taxa from the Indian subcontinent into Southeast Asia, two principal hypotheses have been proposed: the “Biotic-ferry” and “Step-stone” models. The subfamily Perittopinae, a lineage of semi-aquatic bugs comprising a single genus and 20 extant species, provides an ideal system for testing these hypotheses due to its disjunct distribution spanning the Indian subcontinent and Southeast Asia. This study conducted a comprehensive taxonomic analysis of the entire subfamily, incorporating newly defined morphological characters and multilocus phylogenetic analyses to reconstruct evolutionary relationships and historical biogeography. Morphological and phylogenetic evidence confirmed the monophyly of Perittopinae and supported the establishment of three new genera—Indoperittopus gen. nov., Pachyperittopus gen.nov., and Falciperittopus gen. nov.—in addition to four new species and four new combinations. Biogeographic reconstructions indicated a southern Indian origin, with initial diversification potentially occurring during the midPaleocene, coinciding with the major phases of the IndiaEurasia collision. Subsequent range expansion over marine barriers facilitated colonization of the northern Sunda Shelf, consistent with the “Step-stone” dispersal mechanism. Later northward expansion from the southern Sunda Shelf during the early Miocene triggered further diversification of the genus Perittopus within the IndoChina Peninsula. These findings advance understanding of Perittopinae systematics, phylogeny, and historical biogeography, identifying the northward drift of the Indian plate and its eventual collision with Eurasia as catalysts of diversification within this semi-aquatic lineage.

摘要: Chromatin remodeling and transcriptional reprogramming play critical roles during mammalian meiotic prophase I;however, the precise mechanisms regulating these processes remain poorly understood. Our previous work demonstrated that deletion of heat shock factor 5（HSF5）,a member of the heat shock factor family, induces meiotic arrest and male infertility. However, the molecular pathways through which HSF5 governs meiotic progression have not yet been fully elucidated. In this study, a comprehensive multi-omics approach was applied to investigate the role of HSF5 in modulating chromatin dynamics and transcriptional reprogramming during pachynema progression. Analysis of ATAC-seq and singlecell RNA sequencing data revealed significant alterations in chromatin accessibility and disruption of the transcriptional regulatory network（TRN） in Hsf5^-/- spermatocytes. Additionally, HSF5 deficiency resulted in defective XY body formation and altered histone modifications. Notably, Hsf5^-/- spermatocytes also exhibited abnormal spermatoproteasome activity specifically on sex chromosomes, with evidence indicating that HSF5 may form a complex with USP7 in vivo to suppress H2AK119ub on meiotic sex chromosomes.These findings provide new insights into the complex,multifunctional role of HSF5 in regulating key meiotic events and advancing our understanding of its function during pachynema progression.

摘要: 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（E₂） and progesterone（P₄）, which are essential for follicular maturation and ovulatory competence. While circular RNAs（circ RNAs） have been implicated in steroid hormone synthesis, their involvement in the regulation of gilt estrous remains unclear. In this study, circ RNA sequencing was performed on ovarian tissues of estrus（ES） and non-estrus（NES） gilts, resulting in the identification of a novel circ RNA, termed circular SHOC2leucine rich repeat scaffold protein（circSHOC2）, which exhibited marked up-regulation in ES ovaries. Functional assays demonstrated that circSHOC2 overexpression enhanced E₂ and P₄ 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 E₂ and P₄ 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 E₂ and P₄ 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.

摘要: 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 hypoxiainducible factor(HIF) signaling and markedly up-regulating IL-22 expression. IL-22 levels peaked at 24 h posthypoxia, suggesting a role in early immune responses.Recombinant Pf＿IL-22 also induced transcription of proinflammatory 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-1αknockdown. 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.

摘要: 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 BpLEAP2stimulation, 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 promigratory 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 BpLEAP2promotes MO/MΦ migration in teleosts.

摘要: 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 HK1locus under hypoxia, revealing two conserved cisregulatory 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.