Notochord regulates cardiac lineage in zebrafish embryos

被引:55
作者
Goldstein, AM [1 ]
Fishman, MC [1 ]
机构
[1] Massachusetts Gen Hosp E, Cardiovasc Res Ctr, Charlestown, MA 02129 USA
关键词
notochord; cardiac development; Nkx2.5; laser ablation; cell fate; mutants;
D O I
10.1006/dbio.1998.8976
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
We focus here upon regulation by the notochord of myocardial cell fate in zebrafish. Myocardial precursors, defined by lineage tracing in the living embryo, are in the lateral plate mesoderm adjacent to the notochord-prechordal plate junction. Interestingly, the anterior end of the notochord corresponds to the posterior extent of the heart progenitor held, defined by this lineage analysis. This suggested that the notochord might suppress, or the prechordal plate might enhance, the cardiogenic fate. Nkx2.5 expression is, in the zebrafish embryo, closely correlated with the position of myocardial precursors, which reside adjacent to the notochord-prechordal plate junction. This expression, however, is extinguished in the region posterior to this junction, a region normally not contributing cells to the heart. Laser ablation of the notochord tip between the 4-somite and 12-somite stage causes posterior expansion of the Nkx2.5-expressing region. The ntl mutation of the notochord is associated with posterior extension of Nkx2.5 expression. Lineage tracking, by laser activation of caged fluoresceinated dextran, confirms that, normally, lateral plate cells next to the notochord do not contribute progeny to the heart. After anterior notochord ablation, these cells are redirected to a heart cell fate. These data suggest that the anterior notochord delimits the posterior extent of the heart held by suppressing the heart cell fate. (C) 1998 Academic Press.
引用
收藏
页码:247 / 252
页数:6
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