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Mech Dev. 1998 Jun;74(1-2):41-50.

The loss of ventral ectoderm identity correlates with the inability to form an AER in the legless hindlimb bud.

Author information

1
Division of Developmental Biology Children's Hospital Research Foundation, 3333 Burnet Avenue, Cincinnati, OH 45229, USA. sheila.bell@chmcc.org

Abstract

We have characterized the early stages of murine hindlimb morphogenesis in the legless (lgl)mutant and non-mutant littermates. Initially the entire ventral ectoderm expresses many genetic markers characteristic of the AER (en-1, fgf-8, msx-2, dlx-2, cd44, and cx-43). Subsequently, the expression domain of most of these genes is restricted to the thickened ectoderm of the disto-ventral limb margin prior to forming an AER. In lgl, the expression of these genes is initiated but not maintained and the disto-ventral marginal ectoderm does not thicken. In contrast, Wnt7a expression is initiated and maintained in the dorsal ectoderm. The limb mesenchyme of lgl and non-mutant embryos initially expresses lmx-1b and fgf-10 uniformly. As the ventro-distal marginal ectoderm thickens, lmx-1b is progressively dorsally restricted in non-mutants but continues to be expressed ventrally in lgl hindlimb buds. These data suggest that establishment of a dorso-ventral ectodermal interface is not sufficient for AER formation and that restriction of lmx-1b to the dorsal mesenchyme is coordinately linked to AER formation.

PMID:
9651475
DOI:
10.1016/s0925-4773(98)00065-3
[Indexed for MEDLINE]
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