Mutations in PTEN-induced putative kinase 1 ( PINK1) are implicated in early-onset Parkinson's disease (PD). Despite various in vitro studies indicating the importance of PINK1 in mitophagy, its physiological function in the brain remains poorly defined due to undetectable protein levels in rodents and cultured cells under basal conditions. Here, PINK1 was found to be selectively expressed in the primate brain, enabling exploration of its endogenous role invivo. Proteomic profiling via mass spectrometry identified the ubiquitin-conjugating enzyme E2M (UBC12) as a PINK1-interacting partner, with strong colocalization in the monkey brain. Knockdown of PINK1 in monkeys resulted in marked reductions in UBC12 protein abundance and global neddylation, effects not observed in brain tissues from PINK1 knockout mice or pigs. These findings reveal a primate-specific PINK1-UBC12 axis and uncover a previously unrecognized role for PINK1 in protein neddylation, distinct from its established mitophagy function.
{"title":"Regulation of UBC12 expression and protein neddylation by PINK1 suggests a primate-specific function.","authors":"Wei Huang, Ting Xu, Gong-Ke Zhou, Yu-Xuan Li, Chuang-Zhen Lin, Xiu-Sheng Chen, Tong Zhang, Liang Jiang, Yan-Ting Liu, Xin Xiong, Xue-Ying Liang, Xiang-Yu Guo, Shi-Hua Li, Xiao-Jiang Li, Wei-Li Yang","doi":"10.24272/j.issn.2095-8137.2025.106","DOIUrl":"https://doi.org/10.24272/j.issn.2095-8137.2025.106","url":null,"abstract":"<p><p>Mutations in PTEN-induced putative kinase 1 ( <i>PINK1</i>) are implicated in early-onset Parkinson's disease (PD). Despite various <i>in vitro</i> studies indicating the importance of PINK1 in mitophagy, its physiological function in the brain remains poorly defined due to undetectable protein levels in rodents and cultured cells under basal conditions. Here, PINK1 was found to be selectively expressed in the primate brain, enabling exploration of its endogenous role <i>in</i> <i>vivo</i>. Proteomic profiling via mass spectrometry identified the ubiquitin-conjugating enzyme E2M (UBC12) as a PINK1-interacting partner, with strong colocalization in the monkey brain. Knockdown of <i>PINK1</i> in monkeys resulted in marked reductions in UBC12 protein abundance and global neddylation, effects not observed in brain tissues from <i>PINK1</i> knockout mice or pigs. These findings reveal a primate-specific PINK1-UBC12 axis and uncover a previously unrecognized role for PINK1 in protein neddylation, distinct from its established mitophagy function.</p>","PeriodicalId":48636,"journal":{"name":"Zoological Research","volume":"46 6","pages":"1488-1500"},"PeriodicalIF":4.7,"publicationDate":"2025-11-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145641611","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Polycystic ovary syndrome (PCOS), a common female endocrine disorder marked by disrupted folliculogenesis and hyperandrogenism, is increasingly linked to oxidative stress. Despite this association, the mechanistic basis remains poorly characterized. C-Phycocyanin (C-PC), a cyanobacteria-derived protein with potent antioxidant properties, has demonstrated therapeutic potential for treating PCOS, though the molecular pathways mediating its effects have yet to be delineated. This study employed both a dehydroepiandrosterone (DHEA)-induced murine model and DHEA-challenged human granulosa cells (KGN) to elucidate the regulatory role of C-PC. In vivo, oral administration of C-PC restored estrous cyclicity, reduced the prevalence of cystic follicles, and normalized circulating levels of testosterone, estradiol, progesterone, and luteinizing hormone (LH). In vitro, C-PC treatment activated the NRF2/xCT/GPX4 pathway, enhanced antioxidant activity, improved mitochondrial function, and suppressed ferroptotic death. Direct molecular interaction between C-PC and NRF2 was validated through molecular docking and cellular thermal shift assays (CETSA). Correspondingly, in vivo administration alleviated oxidative stress, inhibited ferroptosis, and increased GPX4 and xCT expression, effects reversed by pharmacological inhibition (ML385) and genetic silencing (AAV-sh-NRF2) of NRF2. C-PC also reduced DHEA-induced phosphorylation of AMPK, while co-treatment with an AMPK activator attenuated its effects on GPX4 and xCT, abolishing its anti-ferroptotic protection against granulosa cells. These findings suggest that C-PC mitigates PCOS pathology by repressing granulosa cell ferroptosis through coordinated activation of NRF2 and modulation of redox-sensitive AMPK signaling, highlighting its potential as a redox-targeted therapeutic strategy for PCOS.
{"title":"Rescuing fertility: C-Phycocyanin prevents ovarian damage through NRF2-mediated ferroptosis pathways in polycystic ovary syndrome models.","authors":"Jing Zhang, Qun-Shan Shen, Ya-Xin Chen, Hui-Ru Cheng, Wei Zhang, Ting Xing, Ya-Jing Liu, Yun-Xia Cao, Dan Liang, Man Luo, Biao Yu","doi":"10.24272/j.issn.2095-8137.2025.032","DOIUrl":"https://doi.org/10.24272/j.issn.2095-8137.2025.032","url":null,"abstract":"<p><p>Polycystic ovary syndrome (PCOS), a common female endocrine disorder marked by disrupted folliculogenesis and hyperandrogenism, is increasingly linked to oxidative stress. Despite this association, the mechanistic basis remains poorly characterized. C-Phycocyanin (C-PC), a cyanobacteria-derived protein with potent antioxidant properties, has demonstrated therapeutic potential for treating PCOS, though the molecular pathways mediating its effects have yet to be delineated. This study employed both a dehydroepiandrosterone (DHEA)-induced murine model and DHEA-challenged human granulosa cells (KGN) to elucidate the regulatory role of C-PC. <i>In vivo</i>, oral administration of C-PC restored estrous cyclicity, reduced the prevalence of cystic follicles, and normalized circulating levels of testosterone, estradiol, progesterone, and luteinizing hormone (LH). <i>In vitro</i>, C-PC treatment activated the NRF2/xCT/GPX4 pathway, enhanced antioxidant activity, improved mitochondrial function, and suppressed ferroptotic death. Direct molecular interaction between C-PC and NRF2 was validated through molecular docking and cellular thermal shift assays (CETSA). Correspondingly, <i>in vivo</i> administration alleviated oxidative stress, inhibited ferroptosis, and increased GPX4 and xCT expression, effects reversed by pharmacological inhibition (ML385) and genetic silencing (AAV-sh-NRF2) of NRF2. C-PC also reduced DHEA-induced phosphorylation of AMPK, while co-treatment with an AMPK activator attenuated its effects on GPX4 and xCT, abolishing its anti-ferroptotic protection against granulosa cells. These findings suggest that C-PC mitigates PCOS pathology by repressing granulosa cell ferroptosis through coordinated activation of NRF2 and modulation of redox-sensitive AMPK signaling, highlighting its potential as a redox-targeted therapeutic strategy for PCOS.</p>","PeriodicalId":48636,"journal":{"name":"Zoological Research","volume":"46 6","pages":"1531-1548"},"PeriodicalIF":4.7,"publicationDate":"2025-11-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145649906","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Tau ( MAPT) expression is inversely associated with glioma malignancy and patient survival. However, the molecular mechanisms underlying this correlation are yet to be fully investigated. This study demonstrated that tau suppressed glioma cell proliferation both in vitro and in vivo. Mechanistically, tau promoted fatty acid β-oxidation, leading to DNA damage and glioma cellular senescence. Functional analyses revealed that tau interacted with carnitine palmitoyltransferase 1A (CPT1A), enhancing CPT1 enzymatic activity and thereby accelerating lipid catabolism. These findings establish tau as a regulator of metabolic reprogramming and senescence in glioma via CPT1-dependent β-oxidation and support its potential as a therapeutic target in glioma management.
Tau (MAPT)表达与胶质瘤恶性程度和患者生存率呈负相关。然而,这种相关性背后的分子机制尚未得到充分的研究。本研究表明,tau蛋白在体内和体外均能抑制胶质瘤细胞的增殖。机制上,tau促进脂肪酸β氧化,导致DNA损伤和胶质瘤细胞衰老。功能分析显示,tau蛋白与肉碱棕榈酰基转移酶1A (CPT1A)相互作用,增强CPT1酶活性,从而加速脂质分解代谢。这些发现证实了tau通过cpt1依赖的β-氧化调节神经胶质瘤的代谢重编程和衰老,并支持其作为神经胶质瘤治疗靶点的潜力。
{"title":"Tau impedes glioma progression by enhancing fatty acid β-oxidation-induced cellular senescence.","authors":"Wan-Hong Han, Wu-Jie Zhao, Jia-Wei He, Wen-Peng Zhao, Han-Wen Lu, Zhen-Wei Lu, Xian-Sheng Qiu, Chen Chang, Ya-Ya Zhang, Yuan-Yuan Xie, Yan-Yan Geng, Bing-Chang Zhang, Zhan-Xiang Wang","doi":"10.24272/j.issn.2095-8137.2025.066","DOIUrl":"10.24272/j.issn.2095-8137.2025.066","url":null,"abstract":"<p><p>Tau ( <i>MAPT</i>) expression is inversely associated with glioma malignancy and patient survival. However, the molecular mechanisms underlying this correlation are yet to be fully investigated. This study demonstrated that tau suppressed glioma cell proliferation both <i>in vitro</i> and <i>in vivo</i>. Mechanistically, tau promoted fatty acid β-oxidation, leading to DNA damage and glioma cellular senescence. Functional analyses revealed that tau interacted with carnitine palmitoyltransferase 1A (CPT1A), enhancing CPT1 enzymatic activity and thereby accelerating lipid catabolism. These findings establish tau as a regulator of metabolic reprogramming and senescence in glioma via CPT1-dependent β-oxidation and support its potential as a therapeutic target in glioma management.</p>","PeriodicalId":48636,"journal":{"name":"Zoological Research","volume":"46 6","pages":"1304-1316"},"PeriodicalIF":4.7,"publicationDate":"2025-11-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145410568","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-11-18DOI: 10.24272/j.issn.2095-8137.2025.122
Ling-Yan Yang, Zhi-Liang Lu, David Fernig, Chang-Jun Shi, Rong Rong
Macaques, particularly rhesus ( Macaca mulatta) and cynomolgus ( M. fascicularis) monkeys, are widely utilized in biomedical and toxicological research. Despite their critical role, effective vaccines against many viral pathogens affecting these primates remain limited, and vaccination is generally avoided in experimental populations to prevent potential confounding outcomes. Consequently, maintaining viral control within macaque colonies depends on stringent surveillance, systematic diagnostic testing, and rigorously enforced quarantine protocols. Accurate and early detection of viral infections is therefore essential for colony management and research integrity. This review synthesizes current knowledge on 10 major viruses affecting macaque colonies, outlining their biological characteristics and diagnostic methodologies, and further assesses recent technological advances in viral detection. Drawing upon five years of surveillance data collected by VRL-Asia from breeding facilities across China, this review highlights the prevalence patterns of viral infections among breeding macaques and identifies critical epidemiological trends. These insights provide a valuable reference for researchers, veterinarians, and laboratory personnel seeking to strengthen biosecurity frameworks and ensure the reliability of research involving macaques.
{"title":"Updated practice for detection of viral infections in breeding macaques.","authors":"Ling-Yan Yang, Zhi-Liang Lu, David Fernig, Chang-Jun Shi, Rong Rong","doi":"10.24272/j.issn.2095-8137.2025.122","DOIUrl":"https://doi.org/10.24272/j.issn.2095-8137.2025.122","url":null,"abstract":"<p><p>Macaques, particularly rhesus ( <i>Macaca mulatta</i>) and cynomolgus ( <i>M. fascicularis</i>) monkeys, are widely utilized in biomedical and toxicological research. Despite their critical role, effective vaccines against many viral pathogens affecting these primates remain limited, and vaccination is generally avoided in experimental populations to prevent potential confounding outcomes. Consequently, maintaining viral control within macaque colonies depends on stringent surveillance, systematic diagnostic testing, and rigorously enforced quarantine protocols. Accurate and early detection of viral infections is therefore essential for colony management and research integrity. This review synthesizes current knowledge on 10 major viruses affecting macaque colonies, outlining their biological characteristics and diagnostic methodologies, and further assesses recent technological advances in viral detection. Drawing upon five years of surveillance data collected by VRL-Asia from breeding facilities across China, this review highlights the prevalence patterns of viral infections among breeding macaques and identifies critical epidemiological trends. These insights provide a valuable reference for researchers, veterinarians, and laboratory personnel seeking to strengthen biosecurity frameworks and ensure the reliability of research involving macaques.</p>","PeriodicalId":48636,"journal":{"name":"Zoological Research","volume":"46 6","pages":"1549-1564"},"PeriodicalIF":4.7,"publicationDate":"2025-11-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145649871","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The rapid global dissemination of multidrug-resistant (MDR) bacteria, primarily driven by horizontal gene transfer through conjugative plasmids, poses a significant challenge to modern medicine. Conjugation enables the efficient spread of antibiotic resistance genes across bacterial populations, severely compromising the efficacy of existing therapies. This study examined the inhibitory potential of flavomycin against plasmid-mediated transmission of clinically relevant resistance genes and elucidated the underlying molecular mechanisms. Results showed that flavomycin markedly reduced the conjugative transfer of plasmids carrying blaCTX-M, blaNDM, and mcr-1 genes in a dose-dependent manner, decreasing conjugation frequencies by approximately 14- to 100-fold. Mechanistic analysis indicated that inhibition of plasmid transfer resulted from intracellular depletion of ATP and L-arginine, both essential for the energy-dependent conjugation process. Transcriptomic analyses revealed broad suppression of genes involved in energy metabolism, while supplementation with exogenous L-arginine restored conjugation frequencies. Additionally, flavomycin down-regulated the expression of mating pair formation (MPF) genes and disrupted pilus biogenesis, as confirmed by scanning electron microscopy. These findings identify flavomycin as a potent inhibitor of horizontal gene transfer, acting through disruption of bacterial energy metabolism and impairment of pilus assembly, and highlight its potential as a promising strategy to limit the propagation of MDR bacteria.
{"title":"Flavomycin inhibits plasmid-mediated conjugative transfer of antibiotic resistance genes by disrupting energy metabolism and pilus assembly.","authors":"Yi-Yun Liu, Min Liao, Yu-Jie Li, Cai-Ying Lin, Ruo-Rou Qian, Jing-Hao Liu, Jia-Kuo Chen, Hui-Ying Yue, Xin-Lei Lian, Ying Huang, Jian-Hua Liu","doi":"10.24272/j.issn.2095-8137.2025.125","DOIUrl":"https://doi.org/10.24272/j.issn.2095-8137.2025.125","url":null,"abstract":"<p><p>The rapid global dissemination of multidrug-resistant (MDR) bacteria, primarily driven by horizontal gene transfer through conjugative plasmids, poses a significant challenge to modern medicine. Conjugation enables the efficient spread of antibiotic resistance genes across bacterial populations, severely compromising the efficacy of existing therapies. This study examined the inhibitory potential of flavomycin against plasmid-mediated transmission of clinically relevant resistance genes and elucidated the underlying molecular mechanisms. Results showed that flavomycin markedly reduced the conjugative transfer of plasmids carrying <i>bla</i> <sub>CTX-M</sub>, <i>bla</i> <sub>NDM</sub>, and <i>mcr-1</i> genes in a dose-dependent manner, decreasing conjugation frequencies by approximately 14- to 100-fold. Mechanistic analysis indicated that inhibition of plasmid transfer resulted from intracellular depletion of ATP and L-arginine, both essential for the energy-dependent conjugation process. Transcriptomic analyses revealed broad suppression of genes involved in energy metabolism, while supplementation with exogenous L-arginine restored conjugation frequencies. Additionally, flavomycin down-regulated the expression of mating pair formation (MPF) genes and disrupted pilus biogenesis, as confirmed by scanning electron microscopy. These findings identify flavomycin as a potent inhibitor of horizontal gene transfer, acting through disruption of bacterial energy metabolism and impairment of pilus assembly, and highlight its potential as a promising strategy to limit the propagation of MDR bacteria.</p>","PeriodicalId":48636,"journal":{"name":"Zoological Research","volume":"46 6","pages":"1438-1446"},"PeriodicalIF":4.7,"publicationDate":"2025-11-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145641639","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-11-18DOI: 10.24272/j.issn.2095-8137.2025.349
Yu-Bo Tang, Juan Zhang, Qiang Liu
Transfer ribonucleic acid-derived small ribonucleic acids (tsRNAs) are an emerging class of regulatory noncoding RNAs produced through the precise cleavage of mature or precursor tRNAs (pre-tRNAs). Once considered degradation byproducts, tsRNAs are now recognized as key modulators of gene expression, epigenetic regulation, and cellular stress responses. In recent years, growing evidence has implicated tsRNAs in the aging process of the brain and in the pathogenesis of age-related neurodegenerative diseases, such as Alzheimer's disease (AD), Parkinson's disease (PD), and amyotrophic lateral sclerosis (ALS). These small RNAs are involved in modulating synaptic function, neuronal survival, and neuroinflammation, and their expression profiles are dynamically altered in response to aging and disease-associated stressors. This review summarizes the biogenesis, classification, and molecular and cellular mechanisms of tsRNAs, with an emphasis on their subcellular locations and associated biological functions. We further explore their roles in brain aging and age-related neurodegenerative diseases and the emerging potential of tsRNAs as biomarkers and therapeutic targets for age-related neurological disorders while highlighting current challenges and future directions in this rapidly advancing field.
{"title":"tRNA-derived small noncoding RNAs: Roles in brain aging and neurodegenerative disorders.","authors":"Yu-Bo Tang, Juan Zhang, Qiang Liu","doi":"10.24272/j.issn.2095-8137.2025.349","DOIUrl":"https://doi.org/10.24272/j.issn.2095-8137.2025.349","url":null,"abstract":"<p><p>Transfer ribonucleic acid-derived small ribonucleic acids (tsRNAs) are an emerging class of regulatory noncoding RNAs produced through the precise cleavage of mature or precursor tRNAs (pre-tRNAs). Once considered degradation byproducts, tsRNAs are now recognized as key modulators of gene expression, epigenetic regulation, and cellular stress responses. In recent years, growing evidence has implicated tsRNAs in the aging process of the brain and in the pathogenesis of age-related neurodegenerative diseases, such as Alzheimer's disease (AD), Parkinson's disease (PD), and amyotrophic lateral sclerosis (ALS). These small RNAs are involved in modulating synaptic function, neuronal survival, and neuroinflammation, and their expression profiles are dynamically altered in response to aging and disease-associated stressors. This review summarizes the biogenesis, classification, and molecular and cellular mechanisms of tsRNAs, with an emphasis on their subcellular locations and associated biological functions. We further explore their roles in brain aging and age-related neurodegenerative diseases and the emerging potential of tsRNAs as biomarkers and therapeutic targets for age-related neurological disorders while highlighting current challenges and future directions in this rapidly advancing field.</p>","PeriodicalId":48636,"journal":{"name":"Zoological Research","volume":"46 6","pages":"1575-1587"},"PeriodicalIF":4.7,"publicationDate":"2025-11-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145649828","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-11-18DOI: 10.24272/j.issn.2095-8137.2025.155
Wen-Bo Chen, Cong-Liang Wang, Shi-Cheng Wan, Xuan Luo, Dong-Hui Yang, Meng-Fei Zhang, Wen-Ping Wu, Na Li, Bin Han, Hai-Jing Zhu, Hai-Sheng Yu, Jin-Lian Hua
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.
{"title":"Single-cell transcriptomics reveals dynamic reprogramming of testicular immunity in <i>Brucella</i>-infected goat testis.","authors":"Wen-Bo Chen, Cong-Liang Wang, Shi-Cheng Wan, Xuan Luo, Dong-Hui Yang, Meng-Fei Zhang, Wen-Ping Wu, Na Li, Bin Han, Hai-Jing Zhu, Hai-Sheng Yu, Jin-Lian Hua","doi":"10.24272/j.issn.2095-8137.2025.155","DOIUrl":"https://doi.org/10.24272/j.issn.2095-8137.2025.155","url":null,"abstract":"<p><p>Brucellosis, a zoonotic disease caused by <i>Brucella</i> 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 <i>Brucella</i>-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 ( <i>TXNIP</i>), 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 <i>Brucella</i> infection and highlight candidate targets for immunomodulatory intervention in disease control and livestock reproductive health.</p>","PeriodicalId":48636,"journal":{"name":"Zoological Research","volume":"46 6","pages":"1516-1530"},"PeriodicalIF":4.7,"publicationDate":"2025-11-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145649881","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-11-18DOI: 10.24272/j.issn.2095-8137.2025.229
Xiao-Qing Zhang, Xin-Yu Li, Yuri M Marusik, Mei-Chen Yan, Rui-Han Yang, Ya-Xuan Zhang, Fan-Yu Bu, Yu Ding, Ming-Yue Wang, Zhi-Yuan Yao
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.
{"title":"Spider taxonomy: A historical and global perspective.","authors":"Xiao-Qing Zhang, Xin-Yu Li, Yuri M Marusik, Mei-Chen Yan, Rui-Han Yang, Ya-Xuan Zhang, Fan-Yu Bu, Yu Ding, Ming-Yue Wang, Zhi-Yuan Yao","doi":"10.24272/j.issn.2095-8137.2025.229","DOIUrl":"https://doi.org/10.24272/j.issn.2095-8137.2025.229","url":null,"abstract":"<p><p>Using comprehensive records from the <i>World Spider Catalog</i>, 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 <sup>st</sup> 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 <sup>th</sup> 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.</p>","PeriodicalId":48636,"journal":{"name":"Zoological Research","volume":"46 6","pages":"1387-1395"},"PeriodicalIF":4.7,"publicationDate":"2025-11-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145640933","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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.
{"title":"Multiple lines of evidence for sex-biased dispersal in the nocturnal pitviper <i>Viridovipera stejnegeri</i>.","authors":"Song-Wen Tan, Min Yu, Bing Lyu, Ya-Yong Wu, Guo-Cheng Shu, Qin Liu, Peng Guo","doi":"10.24272/j.issn.2095-8137.2025.212","DOIUrl":"https://doi.org/10.24272/j.issn.2095-8137.2025.212","url":null,"abstract":"<p><p>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 ( <i>Viridovipera stejnegeri</i>) 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 <i>V. stejnegeri</i>, 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.</p>","PeriodicalId":48636,"journal":{"name":"Zoological Research","volume":"46 6","pages":"1477-1487"},"PeriodicalIF":4.7,"publicationDate":"2025-11-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145641673","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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.
{"title":"Whole-brain mapping of monosynaptic afferents to GABAergic neurons in the sublaterodorsal tegmental nucleus of mice.","authors":"Zhi-Gang Zhong, Shang-Qi Tang, Hui Ben, Jia-Lin Yang, Yong-Hua Chen, Wei-Min Qu, Zhi-Li Huang, Mei-Hong Qiu","doi":"10.24272/j.issn.2095-8137.2025.068","DOIUrl":"https://doi.org/10.24272/j.issn.2095-8137.2025.068","url":null,"abstract":"<p><p>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.</p>","PeriodicalId":48636,"journal":{"name":"Zoological Research","volume":"46 6","pages":"1501-1515"},"PeriodicalIF":4.7,"publicationDate":"2025-11-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145649389","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}