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Generation of Myeloid-Specific Bmal1 Knockout Mice and Identification of Bmal1-Regulated Ferroptosis in Macrophages
IF 2.4 4区 生物学
genesis Pub Date : 2025-04-08 DOI: 10.1002/dvg.70014
Qing Chen, Wenyi Wang, Weijun Fang, Lianhua Qin, Jie Wang, Xiaochen Huang, Sha Pan, Ruijuan Zheng
{"title":"Generation of Myeloid-Specific Bmal1 Knockout Mice and Identification of Bmal1-Regulated Ferroptosis in Macrophages","authors":"Qing Chen,&nbsp;Wenyi Wang,&nbsp;Weijun Fang,&nbsp;Lianhua Qin,&nbsp;Jie Wang,&nbsp;Xiaochen Huang,&nbsp;Sha Pan,&nbsp;Ruijuan Zheng","doi":"10.1002/dvg.70014","DOIUrl":"https://doi.org/10.1002/dvg.70014","url":null,"abstract":"<div>\u0000 \u0000 <p>Circadian clocks have a fundamental role in many physiological processes. Bmal1 (basic helix–loop–helix ARNT like 1) is a central master circadian clock gene. The global <i>Bmal1</i> knockout mice were shown to have a loss of circadian rhythms, acceleration of aging, and shortened life span. However, global <i>Bmal1</i> knockout mice did not exactly reflect the Bmal1 function in specific cell or tissue types. To address the importance of circadian rhythms in macrophages, we generated myeloid-specific <i>Bmal1</i> knockout mice. The efficacy of <i>Bmal1</i> gene deletion in macrophages was identified at DNA, transcription, protein levels, and function. In contrast to global <i>Bmal1</i> knockout mice, <i>Bmal1</i><sup><i>flox/flox</i></sup> and <i>Bmal1</i><sup><i>mye−/−</i></sup> mice did not exhibit aging phenotypes. However, the deletion of <i>Bmal1</i> resulted in a loss of rhythmic expression of the circadian genes in macrophages. RNA-Seq revealed that Bmal1 regulated the expression of cell death-related genes in macrophages. Furthermore, these genes have been identified as clock-controlled genes in rhythmic cell models, and Bmal1 controlled the rhythmic expression of these genes in macrophages. Finally, Bmal1 inhibited RSL3-induced ferroptosis in macrophages through Phgdh. In summary, the model of myeloid-specific <i>Bmal1</i> knockout mice was successfully constructed, providing a tool for the study of the roles of Bmal1 in macrophages and the peripheral circadian clock. Meanwhile, Bmal1 regulates ferroptosis in macrophages.</p>\u0000 </div>","PeriodicalId":12718,"journal":{"name":"genesis","volume":"63 2","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143793741","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
CACNA1G, A Heterotaxy Candidate Gene, Plays a Role in Ciliogenesis and Left-Right Patterning in Xenopus tropicalis
IF 2.4 4区 生物学
genesis Pub Date : 2025-02-26 DOI: 10.1002/dvg.70009
Valentyna Kostiuk, Rakib Kabir, Rashid Akbari, Amy Rushing, Delfina P. González, Angelina Kim, Ashley Kim, David Zenisek, Mustafa K. Khokha
{"title":"CACNA1G, A Heterotaxy Candidate Gene, Plays a Role in Ciliogenesis and Left-Right Patterning in Xenopus tropicalis","authors":"Valentyna Kostiuk,&nbsp;Rakib Kabir,&nbsp;Rashid Akbari,&nbsp;Amy Rushing,&nbsp;Delfina P. González,&nbsp;Angelina Kim,&nbsp;Ashley Kim,&nbsp;David Zenisek,&nbsp;Mustafa K. Khokha","doi":"10.1002/dvg.70009","DOIUrl":"https://doi.org/10.1002/dvg.70009","url":null,"abstract":"<div>\u0000 \u0000 <p>Heterotaxy (HTX) is characterized by an abnormality in the organ arrangement along the Left-Right (LR) axis and is caused by the disruption of LR patterning in early development. LR asymmetry is critical for multiple organs. Specifically, proper LR patterning is crucial for cardiac function and is a cause of congenital heart disease (CHD). <i>CACNA1G</i> is a candidate gene identified in patients with CHD and HTX. This gene encodes a T-type, low-voltage-activated calcium channel and is a member of the Cav3.1 channel family. However, its function in cardiac or embryonic development remains unknown. Here, we show that abnormal <i>cacna1g</i> expression in <i>Xenopus tropicalis</i> recapitulates the HTX phenotype found in the patient cohort. By examining early LR patterning markers, including <i>pitx2c</i> and <i>dand5</i>, we discovered that both markers are expressed abnormally, suggesting that LR patterning is disrupted at the earliest stages of the LR signaling cascade. Since cilia have been described as key regulators of LR asymmetry, we checked the process of cilia formation in <i>cacna1g</i> crispants. The LR Organizer (LRO) contained reduced cilia quantity in the <i>cacna1g</i> crispants, which may explain the LR defects. In conclusion, the abnormal expression of <i>cacna1g</i> affects cilia in the LRO, leading to abnormal LR patterning and cardiac looping.</p>\u0000 </div>","PeriodicalId":12718,"journal":{"name":"genesis","volume":"63 1","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143489953","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Meet Our Editorial Board—Genesis. An Interview With Jun (Kelly) Liu, Cornell University, New York, USA 认识我们的编辑委员会--创世纪。美国纽约康奈尔大学刘俊（Kelly）访谈录
IF 2.4 4区 生物学
genesis Pub Date : 2025-02-26 DOI: 10.1002/dvg.70006
Jun (Kelly) Liu, Paul Trevorrow
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引用次数: 0
Meet Our Editorial Board—Genesis: An Interview With Eric Bellefroid, University Libre de Bruxelles, Bruxelles, Belgium
IF 2.4 4区 生物学
genesis Pub Date : 2025-02-26 DOI: 10.1002/dvg.70003
Paul Trevorrow, Eric Bellefroid
{"title":"Meet Our Editorial Board—Genesis: An Interview With Eric Bellefroid, University Libre de Bruxelles, Bruxelles, Belgium","authors":"Paul Trevorrow,&nbsp;Eric Bellefroid","doi":"10.1002/dvg.70003","DOIUrl":"https://doi.org/10.1002/dvg.70003","url":null,"abstract":"","PeriodicalId":12718,"journal":{"name":"genesis","volume":"63 1","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143489841","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Meet Our Editorial Board—Genesis. An Interview With, Mark Lewandoski, National Cancer Institute, Maryland, USA
IF 2.4 4区 生物学
genesis Pub Date : 2025-02-26 DOI: 10.1002/dvg.70007
Mark Lewandoski, Paul Trevorrow
{"title":"Meet Our Editorial Board—Genesis. An Interview With, Mark Lewandoski, National Cancer Institute, Maryland, USA","authors":"Mark Lewandoski,&nbsp;Paul Trevorrow","doi":"10.1002/dvg.70007","DOIUrl":"https://doi.org/10.1002/dvg.70007","url":null,"abstract":"","PeriodicalId":12718,"journal":{"name":"genesis","volume":"63 1","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143489969","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Unraveling the Mechanisms That Regulate Osteoclast Differentiation: A Review of Current Advances
IF 2.4 4区 生物学
genesis Pub Date : 2025-02-17 DOI: 10.1002/dvg.70012
Sai Zhang, Meng Gao, Shuzhe Song, Tongdan Zhao, Bianhua Zhou, Hongwei Wang, Weishun Tian, Wenpeng Zhao, Jing Zhao
{"title":"Unraveling the Mechanisms That Regulate Osteoclast Differentiation: A Review of Current Advances","authors":"Sai Zhang,&nbsp;Meng Gao,&nbsp;Shuzhe Song,&nbsp;Tongdan Zhao,&nbsp;Bianhua Zhou,&nbsp;Hongwei Wang,&nbsp;Weishun Tian,&nbsp;Wenpeng Zhao,&nbsp;Jing Zhao","doi":"10.1002/dvg.70012","DOIUrl":"https://doi.org/10.1002/dvg.70012","url":null,"abstract":"<div>\u0000 \u0000 <p>Osteoporosis is a metabolic bone disease primarily caused by a decreased bone formation and increased bone resorption. Osteoclasts are a special class of terminally differentiated cells that play an important role in normal bone remodeling and bone loss in osteoporosis as well as in a variety of osteolytic diseases. Osteoclasts can be differentiated from monocyte–macrophage cells of the hematopoietic system; they are the key cells in bone resorption. Osteoclast formation and differentiation are regulated by various cytokines and transcription factors. In this review, we summarize recent advances in research on the regulation of osteoclast differentiation and function by factors such as M-CSF, RANKL, AP-1, NFATC1, MITF, and PU.1. Understanding these cytokines and transcription factors can not only help identify targets for osteoclast differentiation but also aid in intervening in the treatment of osteoclast-related diseases.</p>\u0000 </div>","PeriodicalId":12718,"journal":{"name":"genesis","volume":"63 1","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143424119","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
A New Targeted Transgenic Mouse Line for the Study of Protocadherin γC4
IF 2.4 4区 生物学
genesis Pub Date : 2025-02-09 DOI: 10.1002/dvg.70010
Cathy M. McLeod, Camille M. Hanes, Leah C. Fuller, Samjhana Bhandari, Hannah G. Lanthier, Robert W. Burgess, Joshua A. Weiner, Andrew M. Garrett
{"title":"A New Targeted Transgenic Mouse Line for the Study of Protocadherin γC4","authors":"Cathy M. McLeod,&nbsp;Camille M. Hanes,&nbsp;Leah C. Fuller,&nbsp;Samjhana Bhandari,&nbsp;Hannah G. Lanthier,&nbsp;Robert W. Burgess,&nbsp;Joshua A. Weiner,&nbsp;Andrew M. Garrett","doi":"10.1002/dvg.70010","DOIUrl":"https://doi.org/10.1002/dvg.70010","url":null,"abstract":"<div>\u0000 \u0000 <p>The γ-protocadherins (γ-Pcdhs) comprise 22 homophilic cell adhesion molecule isoforms, expressed from the <i>Pcdhg</i> gene cluster via promoter choice mechanisms that serve many crucial functions during neural development. Emerging evidence supports the hypothesis that distinct isoforms have unique functions. The γC4 isoform, which is expressed from the <i>Pcdhgc4</i> promoter and includes its unique variable exon, is the sole γ-Pcdh isoform essential for the postnatal survival in mice. Here we describe a new mouse line (<i>C4-GFP</i>) in which <i>Pcdhgc4</i> with a C-terminal GFP tag is expressed from the <i>Rosa26</i> locus following excision of a lox-Stop-lox cassette by Cre recombinase. We report that restricted expression of this transgene in the nervous system using <i>Nestin-Cre</i> is sufficient to rescue the neonatal lethality of mice mutant for <i>Pcdhgc4</i>. This new line will be a vital tool for dissecting mechanisms underlying the functions of this essential cell adhesion molecule gene, mutations in which have been associated with neurodevelopmental disorders in humans.</p>\u0000 </div>","PeriodicalId":12718,"journal":{"name":"genesis","volume":"63 1","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-02-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143379975","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Meet Our Editorial Board—Genesis. An Interview With, Susan Mackem, National Cancer Institute, Maryland, USA
IF 2.4 4区 生物学
genesis Pub Date : 2025-01-29 DOI: 10.1002/dvg.70011
Paul Trevorrow, Susan Mackem
{"title":"Meet Our Editorial Board—Genesis. An Interview With, Susan Mackem, National Cancer Institute, Maryland, USA","authors":"Paul Trevorrow,&nbsp;Susan Mackem","doi":"10.1002/dvg.70011","DOIUrl":"10.1002/dvg.70011","url":null,"abstract":"","PeriodicalId":12718,"journal":{"name":"genesis","volume":"62 6","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-01-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143068659","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Meet Our Editorial Board—Genesis. An Interview With Yevgenya Grinblat, University of Wisconsin-Madison, Wisconsin, USA
IF 2.4 4区 生物学
genesis Pub Date : 2025-01-27 DOI: 10.1002/dvg.70005
Paul Trevorrow, Yevgenya Grinblat
{"title":"Meet Our Editorial Board—Genesis. An Interview With Yevgenya Grinblat, University of Wisconsin-Madison, Wisconsin, USA","authors":"Paul Trevorrow,&nbsp;Yevgenya Grinblat","doi":"10.1002/dvg.70005","DOIUrl":"10.1002/dvg.70005","url":null,"abstract":"","PeriodicalId":12718,"journal":{"name":"genesis","volume":"62 6","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-01-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143048419","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Meet Our Editorial Board—Genesis. An Interview With Thomas Schimmang, Institute for Biomedicine and Molecular Genetics, Valladolid, Spain
IF 2.4 4区 生物学
genesis Pub Date : 2025-01-27 DOI: 10.1002/dvg.70004
Paul Trevorrow, Thomas Schimmang
{"title":"Meet Our Editorial Board—Genesis. An Interview With Thomas Schimmang, Institute for Biomedicine and Molecular Genetics, Valladolid, Spain","authors":"Paul Trevorrow,&nbsp;Thomas Schimmang","doi":"10.1002/dvg.70004","DOIUrl":"10.1002/dvg.70004","url":null,"abstract":"","PeriodicalId":12718,"journal":{"name":"genesis","volume":"62 6","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-01-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143048398","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
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