{"title":"鸡 TRIM45 的鉴定和表征及其作为 ALV-J 体外复制负调控因子的作用。","authors":"Jiaxing Wang, Qiangzhou Wang, Yuyu Ping, Xuan Huang, Ting Yang, Yulin Bi, Guobin Chang, Shihao Chen","doi":"10.1080/03079457.2024.2419039","DOIUrl":null,"url":null,"abstract":"<p><p>Avian leukosis virus subgroup J (ALV-J) is an alpharetrovirus that infects chickens, causing immunosuppression and a decrease in production performance, leading to substantial economic losses in the poultry industry. ALV-J is also well-known for its oncogenic properties, inducing tumours such as myelomas and haemangiomas in infected chickens. TRIM45 has been identified as a potential tumour suppressor; however, the relationship between TRIM45 expression and ALV-J infection remains to be elucidated. This study aimed to dissect the molecular characteristics of the chicken TRIM45 gene and its modulation during ALV-J infection, as well as its influence on viral replication. We found that the chicken TRIM45 RING domain is significantly different from that of humans and other mammals. TRIM45 is expressed in all chicken tissues, with the highest levels in the heart. Subcellular localization studies indicated a cytoplasmic distribution of TRIM45, forming aggregates within cells. Our findings demonstrate that ALV-J infection significantly upregulates TRIM45 expression in DF-1 cells. To assess the functional role of TRIM45 in ALV-J replication, we employed both gene silencing and overexpression strategies. Strikingly, the overexpression of TRIM45, including a mutant lacking the RING domain, was found to markedly suppress ALV-J replication. In contrast, TRIM45 knockdown via siRNA resulted in an enhanced viral replication, highlighting the importance of TRIM45 limiting ALV-J replication. Mechanistically, overexpression of TRIM45 induces apoptosis in infected cells, independent of its RING domain function. In conclusion, our study demonstrates that chicken TRIM45 acts as a negative regulator of ALV-J replication <i>in vitro</i> by promoting apoptosis in infected cells.<b>RESEARCH HIGHLIGHTS</b>Chicken TRIM45 RING domain and protein localization significantly differ from humans.TRIM45 negatively regulates ALV-J replication <i>in vitro</i>.TRIM45 inhibits ALV-J replication by inducing apoptosis in infected cells.</p>","PeriodicalId":8788,"journal":{"name":"Avian Pathology","volume":" ","pages":"255-264"},"PeriodicalIF":2.5000,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Identification and characterization of chicken TRIM45 and its role as a negative regulator of ALV-J replication <i>in vitro</i>.\",\"authors\":\"Jiaxing Wang, Qiangzhou Wang, Yuyu Ping, Xuan Huang, Ting Yang, Yulin Bi, Guobin Chang, Shihao Chen\",\"doi\":\"10.1080/03079457.2024.2419039\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Avian leukosis virus subgroup J (ALV-J) is an alpharetrovirus that infects chickens, causing immunosuppression and a decrease in production performance, leading to substantial economic losses in the poultry industry. ALV-J is also well-known for its oncogenic properties, inducing tumours such as myelomas and haemangiomas in infected chickens. TRIM45 has been identified as a potential tumour suppressor; however, the relationship between TRIM45 expression and ALV-J infection remains to be elucidated. This study aimed to dissect the molecular characteristics of the chicken TRIM45 gene and its modulation during ALV-J infection, as well as its influence on viral replication. We found that the chicken TRIM45 RING domain is significantly different from that of humans and other mammals. TRIM45 is expressed in all chicken tissues, with the highest levels in the heart. Subcellular localization studies indicated a cytoplasmic distribution of TRIM45, forming aggregates within cells. Our findings demonstrate that ALV-J infection significantly upregulates TRIM45 expression in DF-1 cells. To assess the functional role of TRIM45 in ALV-J replication, we employed both gene silencing and overexpression strategies. Strikingly, the overexpression of TRIM45, including a mutant lacking the RING domain, was found to markedly suppress ALV-J replication. In contrast, TRIM45 knockdown via siRNA resulted in an enhanced viral replication, highlighting the importance of TRIM45 limiting ALV-J replication. Mechanistically, overexpression of TRIM45 induces apoptosis in infected cells, independent of its RING domain function. In conclusion, our study demonstrates that chicken TRIM45 acts as a negative regulator of ALV-J replication <i>in vitro</i> by promoting apoptosis in infected cells.<b>RESEARCH HIGHLIGHTS</b>Chicken TRIM45 RING domain and protein localization significantly differ from humans.TRIM45 negatively regulates ALV-J replication <i>in vitro</i>.TRIM45 inhibits ALV-J replication by inducing apoptosis in infected cells.</p>\",\"PeriodicalId\":8788,\"journal\":{\"name\":\"Avian Pathology\",\"volume\":\" \",\"pages\":\"255-264\"},\"PeriodicalIF\":2.5000,\"publicationDate\":\"2025-04-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Avian Pathology\",\"FirstCategoryId\":\"97\",\"ListUrlMain\":\"https://doi.org/10.1080/03079457.2024.2419039\",\"RegionNum\":2,\"RegionCategory\":\"农林科学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2024/11/8 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"Q1\",\"JCRName\":\"VETERINARY SCIENCES\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Avian Pathology","FirstCategoryId":"97","ListUrlMain":"https://doi.org/10.1080/03079457.2024.2419039","RegionNum":2,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/11/8 0:00:00","PubModel":"Epub","JCR":"Q1","JCRName":"VETERINARY SCIENCES","Score":null,"Total":0}
Identification and characterization of chicken TRIM45 and its role as a negative regulator of ALV-J replication in vitro.
Avian leukosis virus subgroup J (ALV-J) is an alpharetrovirus that infects chickens, causing immunosuppression and a decrease in production performance, leading to substantial economic losses in the poultry industry. ALV-J is also well-known for its oncogenic properties, inducing tumours such as myelomas and haemangiomas in infected chickens. TRIM45 has been identified as a potential tumour suppressor; however, the relationship between TRIM45 expression and ALV-J infection remains to be elucidated. This study aimed to dissect the molecular characteristics of the chicken TRIM45 gene and its modulation during ALV-J infection, as well as its influence on viral replication. We found that the chicken TRIM45 RING domain is significantly different from that of humans and other mammals. TRIM45 is expressed in all chicken tissues, with the highest levels in the heart. Subcellular localization studies indicated a cytoplasmic distribution of TRIM45, forming aggregates within cells. Our findings demonstrate that ALV-J infection significantly upregulates TRIM45 expression in DF-1 cells. To assess the functional role of TRIM45 in ALV-J replication, we employed both gene silencing and overexpression strategies. Strikingly, the overexpression of TRIM45, including a mutant lacking the RING domain, was found to markedly suppress ALV-J replication. In contrast, TRIM45 knockdown via siRNA resulted in an enhanced viral replication, highlighting the importance of TRIM45 limiting ALV-J replication. Mechanistically, overexpression of TRIM45 induces apoptosis in infected cells, independent of its RING domain function. In conclusion, our study demonstrates that chicken TRIM45 acts as a negative regulator of ALV-J replication in vitro by promoting apoptosis in infected cells.RESEARCH HIGHLIGHTSChicken TRIM45 RING domain and protein localization significantly differ from humans.TRIM45 negatively regulates ALV-J replication in vitro.TRIM45 inhibits ALV-J replication by inducing apoptosis in infected cells.
期刊介绍:
Avian Pathology is the official journal of the World Veterinary Poultry Association and, since its first publication in 1972, has been a leading international journal for poultry disease scientists. It publishes material relevant to the entire field of infectious and non-infectious diseases of poultry and other birds. Accepted manuscripts will contribute novel data of interest to an international readership and will add significantly to knowledge and understanding of diseases, old or new. Subject areas include pathology, diagnosis, detection and characterisation of pathogens, infections of possible zoonotic importance, epidemiology, innate and immune responses, vaccines, gene sequences, genetics in relation to disease and physiological and biochemical changes in response to disease. First and subsequent reports of well-recognized diseases within a country are not acceptable unless they also include substantial new information about the disease or pathogen. Manuscripts on wild or pet birds should describe disease or pathogens in a significant number of birds, recognizing/suggesting serious potential impact on that species or that the disease or pathogen is of demonstrable relevance to poultry. Manuscripts on food-borne microorganisms acquired during or after processing, and those that catalogue the occurrence or properties of microorganisms, are unlikely to be considered for publication in the absence of data linking them to avian disease.