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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
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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
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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
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引用次数: 0
Meet Our Editorial Board—Genesis. An Interview With Paolo E. Forni, University at Albany, State University of New York, New York, USA
IF 2.4 4区 生物学
genesis Pub Date : 2025-01-24 DOI: 10.1002/dvg.70002
Paul Trevorrow, Paolo E. Forni
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引用次数: 0
Meet Our Editorial Board—Genesis. An Interview With Yoh-suke Mukouyama, National Institutes of Health, Maryland, USA
IF 2.4 4区 生物学
genesis Pub Date : 2025-01-24 DOI: 10.1002/dvg.70008
Yoh-suke Mukouyama, Paul Trevorrow
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引用次数: 0
Meet Our Editorial Board—Genesis. An Interview With, Sally Moody, The George Washington University School of Medicine and Health Sciences, USA 认识我们的编辑委员会--《创世纪》。专访美国乔治-华盛顿大学医学与健康科学学院莎莉-穆迪。
IF 2.4 4区 生物学
genesis Pub Date : 2024-12-31 DOI: 10.1002/dvg.70000
Paul Trevorrow, Sally A. Moody
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引用次数: 0
Meet Our Editorial Board—Genesis. An Interview With Margot L. K. Williams, Baylor College of Medicine, Texas, USA 见见我们的编辑委员会——创世纪。采访美国德克萨斯州贝勒医学院的玛格特·l·k·威廉姆斯。
IF 2.4 4区 生物学
genesis Pub Date : 2024-12-17 DOI: 10.1002/dvg.70001
Paul Trevorrow, Margot L. K. Williams
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引用次数: 0
Generation and Characterization of a TRIM21 Overexpressing Mouse Line TRIM21过表达小鼠品系的产生和特征描述
IF 2.4 4区 生物学
genesis Pub Date : 2024-11-01 DOI: 10.1002/dvg.23616
Lisa M. Mehlmann, Tracy F. Uliasz, Siu-Pok Yee, Deborah Kaback, Katie M. Lowther
{"title":"Generation and Characterization of a TRIM21 Overexpressing Mouse Line","authors":"Lisa M. Mehlmann,&nbsp;Tracy F. Uliasz,&nbsp;Siu-Pok Yee,&nbsp;Deborah Kaback,&nbsp;Katie M. Lowther","doi":"10.1002/dvg.23616","DOIUrl":"10.1002/dvg.23616","url":null,"abstract":"<p>Specific removal of a protein is a key to understanding its function. “Trim-Away” utilizes TRIM21, an antibody receptor and ubiquitin ligase, for acute and specific reduction of proteins. When TRIM21 is expressed in cells, introduction of a specific antibody causes rapid degradation of the targeted protein; however, TRIM21 is endogenously expressed in few cell types. We have generated a mouse line using CRISPR to insert a conditional overexpression cassette of TRIM21 into the safe harbor site, <i>Rosa26</i>. These conditionally-expressing mice can be bred to a wide variety of <i>Cre</i> mice to target cell-specific TRIM21 overexpression in different tissues. <i>Zp3</i><sup><i>Cre</i></sup> mice expressed TRIM21 protein specifically in oocytes, whereas <i>Hprt</i><sup><i>Cre</i></sup> mice expressed the protein globally. When TRIM21-overexpressing oocytes were microinjected with specific antibodies targeting either the IP<sub>3</sub> receptor or SNAP23, these proteins were effectively degraded. In addition, cortical neural cells from globally-overexpressing TRIM21 mice showed a dramatic reduction in IP<sub>3</sub> receptor protein within hours after electroporation of a specific antibody. These experiments confirm the effectiveness of the Trim-Away method for protein reduction. These mice should make a valuable addition to the broader research community, as a wide range of proteins and cell types can be studied using this method.</p>","PeriodicalId":12718,"journal":{"name":"genesis","volume":"62 5","pages":""},"PeriodicalIF":2.4,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/dvg.23616","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142565116","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Expression and Transcriptional Targets of TGFβ-RII in Paracentrotus lividus Larval Skeletogenesis TGFβ-RII 在红腹角雉幼体骨骼发生过程中的表达和转录靶标
IF 2.4 4区 生物学
genesis Pub Date : 2024-08-14 DOI: 10.1002/dvg.23614
Daniel Goloe, Tsvia Gildor, Smadar Ben-Tabou de-Leon
{"title":"Expression and Transcriptional Targets of TGFβ-RII in Paracentrotus lividus Larval Skeletogenesis","authors":"Daniel Goloe,&nbsp;Tsvia Gildor,&nbsp;Smadar Ben-Tabou de-Leon","doi":"10.1002/dvg.23614","DOIUrl":"10.1002/dvg.23614","url":null,"abstract":"<p>Organisms from the five kingdoms of life use minerals to harden their tissues and make teeth, shells and skeletons, in the process of biomineralization. The sea urchin larval skeleton is an excellent system to study the biological regulation of biomineralization and its evolution. The gene regulatory network (GRN) that controls sea urchin skeletogenesis is known in great details and shows similarity to the GRN that controls vertebrates' vascularization while it is quite distinct from the GRN that drives vertebrates' bone formation. Yet, transforming growth factor beta (TGF-β) signaling regulates both sea urchin and vertebrates' skeletogenesis. Here, we study the upstream regulation and identify transcriptional targets of TGF-β in the Mediterranean Sea urchin species, <i>Paracentrotus lividus.</i> TGF-βRII is transiently active in the skeletogenic cells downstream of vascular endothelial growth factor (VEGF) signaling, in <i>P. lividus</i>. Continuous perturbation of TGF-βRII activity significantly impairs skeletal elongation and the expression of key skeletogenic genes. Perturbation of TGF-βRII after skeletal initiation leads to a delay in skeletal elongation and minor changes in gene expression. TGF-β targets are distinct from its transcriptional targets during vertebrates' bone formation, suggesting that the role of TGF-β in biomineralization in these two phyla results from convergent evolution.</p>","PeriodicalId":12718,"journal":{"name":"genesis","volume":"62 4","pages":""},"PeriodicalIF":2.4,"publicationDate":"2024-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/dvg.23614","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141977034","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Generation of an Armcx1 Conditional Knockout Mouse Armcx1 条件性基因敲除小鼠的产生
IF 2.4 4区 生物学
genesis Pub Date : 2024-08-14 DOI: 10.1002/dvg.23615
Cora L. Bright, Howard M. Bomze, Mantu Bhaumik, Jeremy N. Kay, Romain Cartoni, Sidney M. Gospe III
{"title":"Generation of an Armcx1 Conditional Knockout Mouse","authors":"Cora L. Bright,&nbsp;Howard M. Bomze,&nbsp;Mantu Bhaumik,&nbsp;Jeremy N. Kay,&nbsp;Romain Cartoni,&nbsp;Sidney M. Gospe III","doi":"10.1002/dvg.23615","DOIUrl":"10.1002/dvg.23615","url":null,"abstract":"<div>\u0000 \u0000 <p>Armadillo repeat-containing X-linked protein-1 (Armcx1) is a poorly characterized transmembrane protein that regulates mitochondrial transport in neurons. Its overexpression has been shown to induce neurite outgrowth in embryonic neurons and to promote retinal ganglion cell (RGC) survival and axonal regrowth in a mouse optic nerve crush model. In order to evaluate the functions of endogenous Armcx1 <i>in vivo</i>, we have created a conditional <i>Armcx1</i> knockout mouse line in which the entire coding region of the <i>Armcx1</i> gene is flanked by <i>loxP</i> sites. This <i>Armcx1</i><sup><i>fl</i></sup> line was crossed with mouse strains in which Cre recombinase expression is driven by the promoters for <i>β-actin</i> and <i>Six3</i>, in order to achieve deletion of <i>Armcx1</i> globally and in retinal neurons, respectively. Having confirmed deletion of the gene, we proceeded to characterize the abundance and morphology of RGCs in <i>Armcx1</i> knockout mice aged to 15 months. Under normal physiological conditions, no evidence of aberrant retinal or optic nerve development or RGC degeneration was observed in these mice. The <i>Armcx1</i><sup><i>fl</i></sup> mouse should be valuable for future studies investigating mitochondrial morphology and transport in the absence of Armcx1 and in determining the susceptibility of Armcx1-deficient neurons to degeneration in the setting of additional heritable or environmental stressors.</p>\u0000 </div>","PeriodicalId":12718,"journal":{"name":"genesis","volume":"62 4","pages":""},"PeriodicalIF":2.4,"publicationDate":"2024-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141977035","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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