J4

• 基础研究 • 上一篇    下一篇

小鼠叉头框C2基因变异致室间隔缺损

邓伟国1,付 艳2,3*,谢铁男2,舒 畅2,李玉林3   

  1. 1. 吉林大学公共卫生学院营养与食品卫生学教研室, 吉林 长春130021;2. 吉林大学第一医院妇产科,吉林 长春130021;3. 吉林大学基础医学院病理解剖学教研室,吉林 长春130021
  • 收稿日期:2003-04-17 修回日期:1900-01-01 出版日期:2004-01-28 发布日期:2004-01-28
  • 通讯作者: 付 艳

Ventricular septal defect induced by mutation of mouse Fox C2 gene

DENG Wei-guo1, FU Yan2,3*, XIE Tie-nan2, SHU Chang2,LI Yu-lin3   

  1. 1. Department of Nutrition and Food Hygiene, School of Public Health, Jilin University, Changchun 130021,China;2. Department of Obstetrics and Gynecology, First Hospital, Jilin University,Changchun 130021,China;3. Department of Pathology, School of Basic Medical Sciences, Jilin University,Changchun 130021,China
  • Received:2003-04-17 Revised:1900-01-01 Online:2004-01-28 Published:2004-01-28
  • Contact: FU Yan

摘要: 目的:探讨叉头框C2基因在心血管发生和发育中的作用。方法:通过敲除小鼠叉头框C2基因,解析敲除叉头框C2基因小鼠的心脏发育情况。结果:在98只新生鼠中仅有15只纯合子型叉头框C2基因突变鼠;这些纯合子型动物心脏的室间隔有细小的缝隙连通左右心室;原位杂交显示在10.5 d的胚胎心室内膜有Fox C2 mRNA的表达。结论:敲除叉头框C2基因可使小鼠室间隔发育缺损。

关键词: 遗传学, 叉头框C2, 基因敲除, 小鼠

Abstract: Objective To study the roles of forkhead box C2 (Fox C2) in cardiovascular development. Methods Fox C2-deficient mice were reproduced by targeting mutation and the developmental anomaly in heart was analyzed. Results Of 98 newborns of mice, only 15 ones were homozygotes for Fox C2 mutation. Left and right ventricles of heart were communicated by a tiny crack on ventricular septa in these homozygote animals. In situ hybridization analysis on 10.5 days embryos showed that Fox C2 mRNA expressed at endocardium of ventricle. Conclusion Targeting mutation of Fox C2 gene can result in ventricular septal defect.

Key words: ventricular, genetics, forkhead box C2, gene targeting

中图分类号: 

  • Q786