首页 | 本学科首页   官方微博 | 高级检索  
   检索      


Zebrafish short fin mutations in connexin43 lead to aberrant gap junctional intercellular communication
Authors:Hoptak-Solga Angela D  Klein Kathryn A  DeRosa Adam M  White Thomas W  Iovine M Kathryn
Institution:Lehigh University, Department of Biological Sciences, Iacocca B-217, Bethlehem, PA 18015, USA.
Abstract:Mutations in the zebrafish connexin43 (cx43) gene cause the short fin phenotype, indicating that direct cell-cell communication contributes to bone length. Three independently generated cx43 alleles exhibit short segments of variable sizes, suggesting that gap junctional intercellular communication may regulate bone growth. Dye coupling assays showed that all alleles are capable of forming gap junction channels. However, ionic coupling assays revealed allele-specific differences in coupling efficiency and gating. For instance, oocyte pairs expressing the weakest allele exhibited much higher levels of coupling than either of the strong alleles. Therefore, measurable differences in Cx43 function may be correlated with the severity of defects in bone length.
Keywords:Gap junction  Cx43  Bone growth  Zebrafish  short fin
本文献已被 ScienceDirect PubMed 等数据库收录!
设为首页 | 免责声明 | 关于勤云 | 加入收藏

Copyright©北京勤云科技发展有限公司  京ICP备09084417号