Abstract
Outgrowth and patterning of the vertebrate limb requires a functional apical ectodermal ridge (AER). The AER is a thickening of ectodermal tissue located at the distal end of the limb bud. Loss of this structure, either through genetic or physical manipulations results in truncation of the limb. A number of genes, including Bmps, are expressed in the AER. Previously, it was shown that removal of the BMP receptor Bmpr1a specifically from the AER resulted in complete loss of hindlimbs suggesting that Bmp signaling in the AER is required for limb outgrowth. In this report, we genetically removed the three known AER-expressed Bmp ligands, Bmp2, Bmp4 and Bmp7 from the AER of the limb bud using floxed conditional alleles and the Msx2-cre allele. Surprisingly, only defects in digit patterning and not limb outgrowth were observed. In triple mutants, the anterior and posterior AER was present but loss of the central region of the AER was observed. These data suggest that Bmp ligands expressed in the AER are not required for limb outgrowth but instead play an essential role in maintaining the AER and patterning vertebrate digits.
Highlights
The vertebrate limb begins as a bud of lateral plate mesenchyme surrounded by surface ectoderm
To investigate the role(s) all three Apical Ectodermal Ridge (AER)-expressed Bmp genes play in limb outgrowth and patterning, Bmp2, Bmp4 and Bmp7
Inactivation of the BMP receptor Bmpr1a in the hindlimb AER results in the absence of an AER and the inability to form a hindlimb [12,37]
Summary
The vertebrate limb begins as a bud of lateral plate mesenchyme surrounded by surface ectoderm. Outgrowth of the limb is controlled by the Apical Ectodermal Ridge (AER) This structure resides at the distal end of the limb bud and is composed of a stratified columnar of ectodermal cells [2,3]. Removal of this structure results in truncation of the forming limb [4,5,6]. Fgf appears to be the major factor responsible for limb bud outgrowth since removal of this gene from the AER, but none of the other AER-expressed Fgfs, results in defects in limb patterning [7,8]. Fgf is the most broadly and highly expressed Fgf gene in the AER, which may explain why removal of this gene, but none of the other AER-expressed Fgfs, produces a visible phenotype [10]
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