Zoological Research最新文献

Avian genomes exhibit compact organization and remarkable chromosomal stability. However, the extent and mechanisms by which structural variation in avian genomes differ from those in other vertebrate lineages are poorly explored. This study generated a diploid genome assembly for the golden pheasant ( Chrysolophus pictus), a species distinguished by the vibrant plumage of males. Each haploid genome assembly included complete chromosomal models, incorporating all microchromosomes. Analysis revealed extensive tandem amplification of immune-related genes across the smallest microchromosomes (dot chromosomes), with an average copy number of 54. Structural variation between the haploid genomes was primarily shaped by large insertions and deletions (indels), with minimal contributions from inversions or duplications. Approximately 28% of these large indels were associated with recent insertions of transposable elements, despite their typically low activity in bird genomes. Evidence for significant effects of transposable elements on gene expression was minimal. Evolutionary strata on the sex chromosomes were identified, along with a drastic rearrangement of the W chromosome. These analyses of the high-quality diploid genome of the golden pheasant provide valuable insights into the evolutionary patterns of structural variation in avian genomes.

Somatic cell nuclear transfer (SCNT) has been successfully employed across various mammalian species, yet cloned animals consistently exhibit low pregnancy rates, primarily due to placental abnormalities such as hyperplasia and hypertrophy. This study investigated the involvement of the Hippo signaling pathway in aberrant placental development in SCNT-induced bovine pregnancies. SCNT-derived cattle exhibited placental hypertrophy, including enlarged abdominal circumference and altered placental cotyledon morphology. RNA sequencing analysis indicated significant dysregulation of Hippo signaling pathway genes in SCNT placentas. Co-expression of YAP1 and CCND1 was observed in cloned blastocysts, placental tissues, and bovine placental mesenchymal stem cells (bPMSCs). Manipulation of YAP1 expression demonstrated the capacity to regulate bPMSC proliferation. Experimental assays confirmed the direct binding of YAP1 to CCND1, which subsequently promoted CCND1 expression in bPMSCs. Furthermore, inhibition of CDK6, a downstream target of CCND1, attenuated SCNT bPMSC proliferation. This study identified YAP1 as a key regulatory component within the Hippo signaling pathway that drives placental hyperplasia in cloned cattle through up-regulation of CCND1-CDK6 expression, facilitating cell cycle progression. These findings offer potential avenues for enhancing cloning efficiency, with implications for evolutionary biology and the conservation of valuable germplasm resources.

Substantial evidence points to the early onset of peripheral inflammation in the development of Parkinson's disease (PD), supporting the "body-first" hypothesis. However, there remains a notable absence of PD-specific animal models induced by inflammatory cytokines. This study introduces a novel mouse model of PD driven by the proinflammatory cytokine CXCL1, identified in our previous research. The involvement of CXCL1 in PD pathogenesis was validated using subacute and chronic MPTP-induced mouse models. Based on these findings, 2-month-old C57BL/6J mice were intravenously administered CXCL1 (20 ng/kg/day) for 2 weeks (5 days per week), successfully replicating motor deficits and pathological alterations in the substantia nigra observed in the chronic MPTP model. These results demonstrate the potential of CXCL1-induced inflammation as a mechanism for PD modeling. The model revealed activation of the PPAR signaling pathway in CXCL1-mediated neuronal damage by CXCL1. Linoleic acid, a PPAR-γ activator, significantly mitigated MPTP- and CXCL1-induced toxicity and reduced serum CXCL1 levels. In addition, the CXCL1-injected mouse model shortened the timeline for developing chronic PD mouse model to 2 weeks, offering an efficient platform for studying inflammation-driven processes in PD. The findings provide critical insights into the inflammatory mechanisms underlying PD and identify promising therapeutic targets for intervention.

Animal adaptation to environmental challenges is a complex process involving intricate interactions between the host genotype and gut microbiome composition. The gut microbiome, highly responsive to external environmental factors, plays a crucial role in host adaptability and may facilitate local adaptation within species. Concurrently, the genetic background of host populations influences gut microbiome composition, highlighting the bidirectional relationship between host and microbiome. Despite this, our understanding of gut microbiome plasticity and its role in host adaptability remains limited, particularly in reptiles. To clarify this issue, we conducted a reciprocal translocation experiment with gravid females of the Qinghai toad-headed lizards ( Phrynocephalus vlangalii) between high-altitude (2 600 m a.s.l.) and superhigh-altitude (3 600 m a.s.l.) environments on Dangjin Mountain of the Qinghai-Xizang Plateau, China. One year later, we assessed the phenotypes and gut microbiomes of their offspring. Results revealed significant plasticity in gut microbiome diversity and structure in response to contrasting elevations. High-altitude conditions increased diversity, and maternal effects appeared to enable high-altitude lizards to maintain elevated diversity when exposed to superhigh-altitude environments. Additionally, superhigh-altitude lizards displayed distinct gut microbiome structures with notable host specificity, potentially linked to their lower growth rates. Overall, these findings underscore the importance of the gut microbiome in facilitating reptilian adaptation to rapid environmental changes across altitudinal gradients. Furthermore, this study provides critical insights into microbial mechanisms underpinning local adaptation and adaptative plasticity, offering a foundation for future research on host-microbiome interactions in evolutionary and ecological contexts.

Small RNAs (sRNAs) are a class of molecules capable of perceiving environmental changes and exerting post-transcriptional regulation over target gene expression, thereby influencing bacterial virulence and host immune responses. Pseudomonas plecoglossicida is a pathogenic bacterium that poses a significant threat to aquatic animal health. However, the regulatory mechanisms of sRNAs in P. plecoglossicida remain unclear. This study focused on sRNA113, previously identified as a potential regulator of the fliP gene, a key component of the lateral flagellar type III secretion system. To investigate the effects of sRNA113 on P. plecoglossicida virulence, as well as its role in regulating pathogenic processes and host immune responses, mutant strains lacking this sRNA were generated and analyzed. Deletion of sRNA113 resulted in the up-regulation of lateral flagellar type III secretion system-related genes in P. plecoglossicida, which enhanced bacterial swarming motility, biofilm formation, and chemotaxis ability in vitro. In vivo infection experiments with pearl gentian grouper revealed that sRNA113 deletion enhanced the pathogenicity of P. plecoglossicida. This heightened virulence was attributed to the up-regulation of genes associated with the lateral flagellar type III secretion system, resulting in higher bacterial loads within host tissues. This amplification of pathogenic activity intensified tissue damage, disrupted immune responses, and impaired the ability of the host to clear infection, ultimately leading to mortality. These findings underscore the critical role of sRNA113 in regulating the virulence of P. plecoglossicida and its interaction with host immune defenses. This study provides a foundation for further exploration of sRNA-mediated mechanisms in bacterial pathogenesis and host-pathogen interactions, contributing to a deeper understanding of virulence regulation and immune evasion in aquatic pathogens.

Pigeons and certain other avian species produce a milk-like secretion in their crop sacs to nourish offspring, yet the detailed processes involved are not fully elucidated. This study investigated the crop sacs of 225-day-old unpaired non-lactating male pigeons (MN) and males initiating lactation on the first day after incubation (ML). Using RNA sequencing, ribosome profiling, and single-cell transcriptome sequencing (scRNA-seq), we identified a significant up-regulation of genes associated with ribosome assembly and protein synthesis in ML compared to MN. Results from scRNA-seq analysis identified 12 distinct cell types and 22 clusters, with secretory epithelial cells (SECs) exhibiting marked expression of plasma cell markers, including IGLL1 and MZB1. RNA fluorescence in situ hybridization (RNA FISH) and IgY quantification confirmed the critical role of SECs in producing endogenous IgY during lactation. We propose that fibroblast-derived BAFF signals activate SECs, mimicking B cell transformation and enhancing protein production through the unfolded protein response (UPR). These findings shed light on the cellular dynamics of pigeon milk production and contribute to a broader understanding of avian biology.

Polystyrene nanoparticles pose significant toxicological risks to aquatic ecosystems, yet their impact on zebrafish ( Danio rerio) embryonic development, particularly erythropoiesis, remains underexplored. This study used single-cell RNA sequencing to comprehensively evaluate the effects of polystyrene nanoparticle exposure on erythropoiesis in zebrafish embryos. In vivo validation experiments corroborated the transcriptomic findings, revealing that polystyrene nanoparticle exposure disrupted erythrocyte differentiation, as evidenced by the decrease in mature erythrocytes and concomitant increase in immature erythrocytes. Additionally, impaired heme synthesis further contributed to the diminished erythrocyte population. These findings underscore the toxic effects of polystyrene nanoparticles on hematopoietic processes, highlighting their potential to compromise organismal health in aquatic environments.

DNA2, a multifunctional enzyme with structure-specific nuclease, 5 '-to-3 ' helicase, and DNA-dependent ATPase activities, plays a pivotal role in the cellular response to DNA damage. However, its involvement in cerebral ischemia/reperfusion (I/R) injury remains to be elucidated. This study investigated the involvement of DNA2 in cerebral I/R injury using conditional knockout (cKO) mice ( Nestin-Cre) subjected to middle cerebral artery occlusion (MCAO), an established model of cerebral I/R. Results demonstrated a gradual up-regulation of DNA2 expression, peaking at 72 h post-MCAO. Notably, DNA2 cKO mice exhibited more pronounced brain injury, neurological deficits, and neuronal apoptosis within the penumbra following MCAO. Additionally, DNA2 expression was elevated in an oxygen-glucose deprivation/reoxygenation (OGD/R) cell culture model, and DNA2 knockdown (KD) exacerbated neuronal apoptosis and oxidative stress. Transcriptome analysis of ischemic penumbra tissues via RNA sequencing revealed significant down-regulation of Homer1 in DNA2 cKO mice. Furthermore, in vitro experiments demonstrated that overexpression of Homer1a ameliorated DNA2 KD-induced neuronal apoptosis. Collectively, these findings demonstrate that DNA2 deficiency exacerbates cerebral I/R injury through the down-regulation of Homer1a, highlighting a novel regulatory axis in ischemic neuroprotection.

The amniote pallium, a vital component of the forebrain, exhibits considerable evolutionary divergence across species and mediates diverse functions, including sensory processing, memory formation, and learning. However, the relationships among pallial subregions in different species remain poorly characterized, particularly regarding the identification of homologous neurons and their transcriptional signatures. In this study, we utilized single-nucleus RNA sequencing to examine over 130 000 nuclei from the macaque ( Macaca fascicularis) neocortex, complemented by datasets from humans ( Homo sapiens), mice ( Mus musculus), zebra finches ( Taeniopygia guttata), turtles ( Chrysemys picta bellii), and lizards ( Pogona vitticeps), enabling comprehensive cross-species comparison. Results revealed transcriptomic conservation and species-specific distinctions within the amniote pallium. Notable similarities were observed among cell subtypes, particularly within PVALB ⁺ inhibitory neurons, which exhibited species-preferred subtypes. Furthermore, correlations between pallial subregions and several transcription factor candidates were identified, including RARB, DLX2, STAT6, NR3C1, and THRB, with potential regulatory roles in gene expression in mammalian pallial neurons compared to their avian and reptilian counterparts. These results highlight the conserved nature of inhibitory neurons, remarkable regional divergence of excitatory neurons, and species-specific gene expression and regulation in amniote pallial neurons. Collectively, these findings provide valuable insights into the evolutionary dynamics of the amniote pallium.

Feeding behavior is regulated by a complex network of endogenous neuropeptides. In chordates, this role is suggested to be under the control of diverse factors including thyrotropin-releasing hormone (TRH). However, whether this regulatory activity of TRH is functionally conserved in non-chordate metazoans, and to what extent this process is underpinned by interactions of TRH with other neuropeptides such as cholecystokinin (CCK, known as a satiety signal), remain unclear. This study investigated the TRH signaling system in the echinoderm Apostichopus japonicus. Bioinformatic analyses and ligand-binding assays identified a functional TRH receptor (AjTRHR) that activated signaling via the MAPK/ERK1/2 pathways. Experimental administration of TRH significantly reduced feeding activity, while up-regulating CCK expression. RNA interference (RNAi) experiments confirmed that both CCK and TRH are essential components of satiety signaling, working synergistically to mediate feeding inhibition. Evolutionary analysis of TRH-type peptides revealed greater conservation of the short isoform of TRH compared to the long isoform, probably driven by strong selection acting on the functional redundancy. These findings provide compelling evidence of a TRH-mediated signaling system in non-chordate deuterostomes, expanding our understanding of neuropeptide-regulated feeding mechanisms in marine invertebrates.