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动物学研究
中国科学院昆明动物研究所 中国动物学会
动物学研究

中国科学院昆明动物研究所 中国动物学会

姚永刚

双月刊

0254-5853

zoores@mail.kiz.ac.cn

0871-65199026

650223

昆明市教场东路32号中国科学院昆明动物研究所

动物学研究/Journal Zoological ResearchCSCD北大核心CSTPCDSCI
查看更多>>本刊创刊于1980年。是中国科学院昆明动物研究所主办的向国内外公开发行的学报级学术性期刊。以报道我国动物学领域的新成果、新进展为已任。在《中文核心期刊要目总览》中多次被列为动物学类核心期刊。本刊辟有研究论文、综述、简报、通讯、书评等栏目，主要刊登动物学领域各分支学科有创新性的基础和应用基础研究报告；结合本人研究工作，反映国际最新研究水平的综述；研究简报、快报；新书评介等。近年发表论文中，动物生态医学、进化生物学分别占30%以上。本刊读者对象为科研机构、大专院校从事动物学研究、教学以及资源环境保护与管理的有关人员；也可为从事生命科学、医学、农林牧渔等方面的科研、教学和生产管理人员提供参考资料。
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    Insights into the genetic architecture of congenital heart disease from animal modeling

    Wenjuan ZhuCecilia W.Lo
    577-590页
    查看更多>>摘要：Congenital heart disease (CHD) is observed in up to 1％ of live births and is one of the leading causes of mortality from birth defects. While hundreds of genes have been implicated in the genetic etiology of CHD, their role in CHD pathogenesis is still poorly understood. This is largely a reflection of the sporadic nature of CHD, as well as its variable expressivity and incomplete penetrance. We reviewed the monogenic causes and evidence for oligogenic etiology of CHD, as well as the role of de novo mutations, common variants, and genetic modifiers. For further mechanistic insight, we leveraged single-cell data across species to investigate the cellular expression characteristics of genes implicated in CHD in developing human and mouse embryonic hearts. Understanding the genetic etiology of CHD may enable the application of precision medicine and prenatal diagnosis, thereby facilitating early intervention to improve outcomes for patients with CHD.
      原文链接:
    • 万方数据
    • 维普

    Large animal models of cardiac ischemia-reperfusion injury:Where are we now?

    Attaur RahmanYuhao LiTo-Kiu ChanHui Zhao...
    591-603页
    查看更多>>摘要：Large animal models of cardiac ischemia-reperfusion are critical for evaluation of the efficacy of cardioprotective interventions prior to clinical translation. Nonetheless,current cardioprotective strategies/interventions formulated in preclinical cardiovascular research are often limited to small animal models, which are not transferable or reproducible in large animal models due to different factors such as: (ⅰ) complex and varied features of human ischemic cardiac disease (ICD), which are challenging to mimic in animal models, (ⅱ) significant differences in surgical techniques applied, and (ⅲ) differences in cardiovascular anatomy and physiology between small versus large animals. This article highlights the advantages and disadvantages of different large animal models of preclinical cardiac ischemic reperfusion injury(IRI), as well as the different methods used to induce and assess IRI, and the obstacles faced in using large animals for translational research in the settings of cardiac IR.
      原文链接:
    • 万方数据

    Gradient descent decomposition of force-field motor primitives optogenetically elicited for motor mapping of the murine lumbosacral spinal cord

    Paola SalmasVincent C.K Cheung
    604-619页
    查看更多>>摘要：Generating diverse motor behaviors critical for survival is a challenge that confronts the central nervous system (CNS)of all animals. During movement execution, the CNS performs complex calculations to control a large number of neuromusculoskeletal elements. The theory of modular motor control proposes that spinal interneurons are organized in discrete modules that can be linearly combined to generate a variety of behavioral patterns.These modules have been previously represented as stimulus-evoked force fields (FFs) comprising isometric limb-endpoint forces across workspace locations. Here, we ask whether FFs elicited by different stimulations indeed represent the most elementary units of motor control or are themselves the combination of a limited number of even more fundamental motor modules. To probe for potentially more elementary modules, we optogenetically stimulated the lumbosacral spinal cord of intact and spinalized Thy1-ChR2 transgenic mice (n=21), eliciting FFs from as many single stimulation loci as possible (20-70 loci per mouse)at minimally necessary power. We found that the resulting varieties of FFs defied simple categorization with just a few clusters. We used gradient descent to further decompose the FFs into their underlying basic force fields (BFFs),whose linear combination explained FF variability. Across mice, we identified 4-5 BFFs with partially localizable but overlapping representations along the spinal cord. The BFFs were structured and topographically distributed in such a way that a rostral-to-caudal traveling wave of activity across the lumbosacral spinal cord may generate a swing-to-stance gait cycle. These BFFs may represent more rudimentary submodules that can be flexibly merged to produce a library of motor modules for building different motor behaviors.
      原文链接:
    • 万方数据
    • 维普

    Extracellular vesicles from iPSC-MSCs alleviate chemotherapy-induced mouse ovarian damage via the ILK-PI3K/AKT pathway

    Rui-Can CaoYue LvGang LuHong-Bin Liu...
    620-635页
    查看更多>>摘要：Chemotherapy can significantly reduce follicle counts in ovarian tissues and damage ovarian stroma, causing endocrine disorder, reproductive dysfunction, and primary ovarian insufficiency (POI). Recent studies have suggested that extracellular vesicles (EVs) secreted from mesenchymal stem cells (MSCs) exert therapeutic effects in various degenerative diseases. In this study,transplantation of EVs from human induced pluripotent stem cell-derived MSCs (iPSC-MSC-EVs) resulted in significant restoration of ovarian follicle numbers, improved granulosa cell proliferation, and inhibition of apoptosis in chemotherapy-damaged granulosa cells, cultured ovaries,and in vivo ovaries in mice. Mechanistically, treatment with iPSC-MSC-EVs resulted in up-regulation of the integrin-linked kinase (ILK) -PI3K/AKT pathway, which is suppressed during chemotherapy, most likely through the transfer of regulatory microRNAs (miRNAs) targeting ILK pathway genes. This work provides a framework for the development of advanced therapeutics to ameliorate ovarian damage and POI in female chemotherapy patients.
      原文链接:
    • 万方数据
    • 维普

    EPAS1 prevents telomeric damage-induced senescence by enhancing transcription of TRF1,TRF2,and RAD50

    Kai-Qin LiGao-Jing LiuXiu-Yun LiuQiong-Fang Chen...
    636-649页
    查看更多>>摘要：Telomeres are nucleoprotein structures located at the end of each chromosome, which function in terminal protection and genomic stability. Telomeric damage is closely related to replicative senescence in vitro and physical aging in vivo. As relatively long-lived mammals based on body size,bats display unique telomeric patterns, including the up-regulation of genes involved in alternative lengthening of telomeres (ALT), DNA repair, and DNA replication. At present, however, the relevant molecular mechanisms remain unclear. In this study, we performed cross-species comparison and identified EPAS1, a well-defined oxygen response gene, as a key telomeric protector in bat fibroblasts. Bat fibroblasts showed high expression of EPAS1, which enhanced the transcription of shelterin components TRF1 and TRF2, as well as DNA repair factor RAD50, conferring bat fibroblasts with resistance to senescence during long-term consecutive expansion.Based on a human single-cell transcriptome atlas, we found that EPAS1 was predominantly expressed in the human pulmonary endothelial cell subpopulation. Using in vitro-cultured human pulmonary endothelial cells, we confirmed the functional and mechanistic conservation of EPAS1 in telomeric protection between bats and humans.In addition, the EPAS1 agonist M1001 was shown to be a protective compound against bleomycin-induced pulmonary telomeric damage and senescence. In conclusion, we identified a potential mechanism for regulating telomere stability in human pulmonary diseases associated with aging, drawing insights from the longevity of bats.
      原文链接:
    • 万方数据
    • 维普

    Decoding hereditary spastic paraplegia pathogenicity through transcriptomic profiling

    Nicolas James HoXiao ChenYong LeiShen Gu...
    650-662页
    查看更多>>摘要：Hereditary spastic paraplegia (HSP) is a group of genetic motor neuron diseases resulting from length-dependent axonal degeneration of the corticospinal upper motor neurons. Due to the advancement of next-generation sequencing, more than 70 novel HSP disease-causing genes have been identified in the past decade. Despite this, our understanding of HSP physiopathology and the development of efficient management and treatment strategies remain poor. One major challenge in studying HSP pathogenicity is selective neuronal vulnerability,characterized by the manifestation of clinical symptoms that are restricted to specific neuronal populations, despite the presence of germline disease-causing variants in every cell of the patient. Furthermore, disease genes may exhibit ubiquitous expression patterns and involve a myriad of different pathways to cause motor neuron degeneration. In the current review, we explore the correlation between transcriptomic data and clinical manifestations, as well as the importance of interspecies models by comparing tissue-specific transcriptomic profiles of humans and mice,expression patterns of different genes in the brain during development, and single-cell transcriptomic data from related tissues. Furthermore, we discuss the potential of emerging single-cell RNA sequencing technologies to resolve unanswered questions related to HSP pathogenicity.
      原文链接:
    • 万方数据
    • 维普

    Genome-wide identification and spatiotemporal expression profiling of zinc finger SWIM domain-containing protein family genes

    Imtiaz UI HassanHafiz Mamoon RehmanZiran LiuLiangji Zhou...
    663-674页
    查看更多>>摘要：The biological function of the novel zinc-finger SWIM domain-containing protein family (ZSWIM) during embryonic development remains elusive. Here, we conducted a genome-wide analysis to explore the evolutionary processes of the ZSWIM gene family members in mice, Xenopus tropicalis, zebrafish, and humans. We identified nine putative ZSWIM genes in the human and mouse genome, eight in the Xenopus genome,and five in the zebrafish genome. Based on multiple sequence alignment, three members, ZSWIM5, ZSWIM6,and ZSWIM8, demonstrated the highest homology across all four species. Using available RNA sequencing (RNA-seq) data, ZSWIM genes were found to be widely expressed across different tissues, with distinct tissue-specific properties. To identify the functions of the ZSWIM protein family during embryogenesis, we examined temporal and spatial expression patterns of zswim family genes in Xenopus embryos. Quantitative real-time polymerase chain reaction (qRT-PCR) revealed that each member had a distinct expression profile. Whole-mount in situ hybridization showed that both zswim1 and zswim3 were maternally expressed genes; zswim5 and zswim6 were expressed throughout embryogenesis and displayed dynamic expression in the brain, eyes, somite, and bronchial arch at the late tailbud stages; zswim7 was detected in the eye area; zswim8 showed a dynamic expression pattern during the tailbud stages, with expression detected in the brain, eyes, and somite;zswim9 was faintly expressed throughout embryonic development. This study provides a foundation for future research to delineate the functions of ZSWIM gene members.
      原文链接:
    • 万方数据
    • 维普

    Zoological Research Call for Papers: Special Issue on Single-Cell and Spatial-Omics

    后插1页
      原文链接:
    • 万方数据