1. Academic Validation
  2. Alterations in somite patterning of Myf-5-deficient mice: a possible role for FGF-4 and FGF-6

Alterations in somite patterning of Myf-5-deficient mice: a possible role for FGF-4 and FGF-6

  • Development. 1996 Jan;122(1):141-50. doi: 10.1242/dev.122.1.141.
S Grass 1 H H Arnold T Braun
Affiliations

Affiliation

  • 1 Department of Cell and Molecular Biology, University of Braunschweig, Germany.
Abstract

Mice carrying a targeted mutation in the gene for the myogenic factor Myf-5 fail to form major parts of the ribs, which leads to an unstable thorax and perinatal death. Here, we report that somites of Myf-5-deficient mice lack the expression of FGF-4 and FGF-6 while TGF beta-2 is expressed normally. Early sclerotomal markers, such as Pax-1 reveal no substantial reduction of sclerotome size. At E11.5 the condensing mesenchyme of the rib anlagen is considerably reduced in size in Myf-5 mutant mice. This may be caused by the lack of Myf-5-positive, FGF-expressing cells which normally are in close contact with the lateral sclerotome generating the rib progenitors. The potential role of FGFs and TGF beta on sclerotome formation is demonstrated in micromass cultures of early somites. Combinations of FGF-4 or FGF-6 with TGF beta-2 potentiate chondrogenesis suggesting that these growth factors emanating from early myotomal and dermomyotomal cells may have instructive or permissive effects on differentiation or outgrowth of sclerotomal cells.

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