CARDIAC MALFORMATION IN NEONATAL MICE LACKING CONNEXIN43

被引:1045
作者
REAUME, AG
DESOUSA, PA
KULKARNI, S
LANGILLE, BL
ZHU, DG
DAVIES, TC
JUNEJA, SC
KIDDER, GM
ROSSANT, J
机构
[1] MT SINAI HOSP, SAMUEL LUNENFELD RES INST, TORONTO, ON M5G 1X5, CANADA
[2] UNIV TORONTO, DEPT MOLEC & MED GENET, TORONTO, ON M5S 1A8, CANADA
[3] UNIV WESTERN ONTARIO, DEPT ZOOL, LONDON, ON N6A 5B7, CANADA
[4] UNIV WESTERN ONTARIO, MOLEC GENET UNIT, LONDON, ON N6A 5B7, CANADA
[5] MAX BELL RES CTR, TORONTO GEN DIV, TORONTO, ON M5G 2C4, CANADA
[6] UNIV TORONTO, DEPT PATHOL, TORONTO, ON M5S 1A8, CANADA
关键词
D O I
10.1126/science.7892609
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Gap junctions are made up of connexin proteins, which comprise a multigene family in mammals. Targeted mutagenesis of connexin43 (Cx43), one of the most prevalent connexin proteins, showed that its absence was compatible with survival of mouse embryos to term, even though mutant cell lines showed reduced dye coupling in vitro. However, mutant embryos died at birth, as a result of a failure in pulmonary gas exchange caused by a swelling and blockage of the right ventricular outflow tract from the heart. This finding suggests that Cx43 plays an essential role in heart development but that there is functional compensation among connexins in other parts of the developing fetus.
引用
收藏
页码:1831 / 1834
页数:4
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