Zebrafish short fin mutations in connexin43 lead to aberrant gap junctional intercellular communication

被引:31
作者
Hoptak-Solga, Angela D.
Klein, Kathryn A.
DeRosa, Adam M.
White, Thomas W.
Iovine, M. Kathryn
机构
[1] Lehigh Univ, Dept Sci Biol, Bethlehem, PA 18015 USA
[2] SUNY Stony Brook, Grad Program Genet, Stony Brook, NY 11794 USA
[3] SUNY Stony Brook, Dept Physiol & Biophys, Stony Brook, NY 11794 USA
来源
FEBS LETTERS | 2007年 / 581卷 / 17期
关键词
gap junction; Cx43; bone growth; zebrafish; short fin;
D O I
10.1016/j.febslet.2007.06.030
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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. (C) 2007 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
引用
收藏
页码:3297 / 3302
页数:6
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