Alexander W. Seaver, Xinxhao Li, M. Kathryn Iovine
{"title":"钾通道Kcna5的过度表达改变了斑马鱼再生鳍的骨骼模式。","authors":"Alexander W. Seaver, Xinxhao Li, M. Kathryn Iovine","doi":"10.1016/j.ydbio.2025.09.001","DOIUrl":null,"url":null,"abstract":"<div><div>Skeletal patterning relies on a complex network of molecular and genetic regulators. However, our understanding of pathways governing joint placement and morphogenesis remains incomplete. Prior studies have demonstrated that medially located Cx43 mediated gap junctional intercellular communication (GJIC) inhibits joint formation by the adjacent lateral skeletal precursor cells, and thereby determines skeletal patterning in the teleost regenerating fin. Here, we test the model that Cx43-GJIC regulates joint formation by propagating changes in membrane potential (ΔV<sub>m</sub>). To provide evidence that ΔV<sub>m</sub> is sufficient to influence joint formation, we generated a transgenic line that expresses the <em>X. laevis voltage-gated channel, shaker-related subfamily, member 5</em> (<em>kcna5</em>) behind the temperature-inducible <em>heat shock protein 70</em> (<em>hsp70</em>) promoter. Using this line, we demonstrate that <em>Xl</em>-<em>kcna5</em> overexpression delays <em>evx1</em> expression and causes longer segments. Moreover, the increased segment length in response to Xl-Kcna5 overexpression requires Cx43. These findings support a model whereby potassium channels act together with gap junction channels to influence joint formation, and therefore skeletal patterning, in the zebrafish regenerating fin.</div></div>","PeriodicalId":11070,"journal":{"name":"Developmental biology","volume":"528 ","pages":"Pages 57-65"},"PeriodicalIF":2.1000,"publicationDate":"2025-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Overexpression of potassium channel Kcna5 alters skeletal patterning in the zebrafish regenerating fin\",\"authors\":\"Alexander W. Seaver, Xinxhao Li, M. Kathryn Iovine\",\"doi\":\"10.1016/j.ydbio.2025.09.001\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><div>Skeletal patterning relies on a complex network of molecular and genetic regulators. However, our understanding of pathways governing joint placement and morphogenesis remains incomplete. Prior studies have demonstrated that medially located Cx43 mediated gap junctional intercellular communication (GJIC) inhibits joint formation by the adjacent lateral skeletal precursor cells, and thereby determines skeletal patterning in the teleost regenerating fin. Here, we test the model that Cx43-GJIC regulates joint formation by propagating changes in membrane potential (ΔV<sub>m</sub>). To provide evidence that ΔV<sub>m</sub> is sufficient to influence joint formation, we generated a transgenic line that expresses the <em>X. laevis voltage-gated channel, shaker-related subfamily, member 5</em> (<em>kcna5</em>) behind the temperature-inducible <em>heat shock protein 70</em> (<em>hsp70</em>) promoter. Using this line, we demonstrate that <em>Xl</em>-<em>kcna5</em> overexpression delays <em>evx1</em> expression and causes longer segments. Moreover, the increased segment length in response to Xl-Kcna5 overexpression requires Cx43. These findings support a model whereby potassium channels act together with gap junction channels to influence joint formation, and therefore skeletal patterning, in the zebrafish regenerating fin.</div></div>\",\"PeriodicalId\":11070,\"journal\":{\"name\":\"Developmental biology\",\"volume\":\"528 \",\"pages\":\"Pages 57-65\"},\"PeriodicalIF\":2.1000,\"publicationDate\":\"2025-09-03\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Developmental biology\",\"FirstCategoryId\":\"99\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S001216062500243X\",\"RegionNum\":3,\"RegionCategory\":\"生物学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"DEVELOPMENTAL BIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Developmental biology","FirstCategoryId":"99","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S001216062500243X","RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"DEVELOPMENTAL BIOLOGY","Score":null,"Total":0}
Overexpression of potassium channel Kcna5 alters skeletal patterning in the zebrafish regenerating fin
Skeletal patterning relies on a complex network of molecular and genetic regulators. However, our understanding of pathways governing joint placement and morphogenesis remains incomplete. Prior studies have demonstrated that medially located Cx43 mediated gap junctional intercellular communication (GJIC) inhibits joint formation by the adjacent lateral skeletal precursor cells, and thereby determines skeletal patterning in the teleost regenerating fin. Here, we test the model that Cx43-GJIC regulates joint formation by propagating changes in membrane potential (ΔVm). To provide evidence that ΔVm is sufficient to influence joint formation, we generated a transgenic line that expresses the X. laevis voltage-gated channel, shaker-related subfamily, member 5 (kcna5) behind the temperature-inducible heat shock protein 70 (hsp70) promoter. Using this line, we demonstrate that Xl-kcna5 overexpression delays evx1 expression and causes longer segments. Moreover, the increased segment length in response to Xl-Kcna5 overexpression requires Cx43. These findings support a model whereby potassium channels act together with gap junction channels to influence joint formation, and therefore skeletal patterning, in the zebrafish regenerating fin.
期刊介绍:
Developmental Biology (DB) publishes original research on mechanisms of development, differentiation, and growth in animals and plants at the molecular, cellular, genetic and evolutionary levels. Areas of particular emphasis include transcriptional control mechanisms, embryonic patterning, cell-cell interactions, growth factors and signal transduction, and regulatory hierarchies in developing plants and animals.