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Inactivation of FGF8 in early mesoderm reveals an essential role in kidney development

  1. Author:
    Perantoni, A. O.
    Timofeeva, O.
    Naillat, F.
    Richman, C.
    Pajni-Underwood, S.
    Wilson, C.
    Vainio, S.
    Dove, L. F.
    Lewandoski, M.

  2. Author Address

    NCI, Canc & Dev Biol Lab, Frederick, MD 21702 USA. NCI, Lab Comparat Carcinogenesis, Frederick, MD 21702 USA. Univ Oulu, Dept Med Biochem & Mol Biol, FIN-90014 Oulu, Finland. Univ Oulu, Bioctr Oulu, FIN-90014 Oulu, Finland Lewandoski, M, NCI, Canc & Dev Biol Lab, Frederick, MD 21702 USA
    1. Year: 2005
    2. Date: SEP
  2. Journal: Development
    1. 132
    2. 17
    3. Pages: 3859-3871
  4. Type of Article: Article
  1. Abstract:

    To bypass the essential gastrulation function of Fgf8 and study its role in lineages of the primitive streak, we have used a new mouse line, T-Cre, to generate mouse embryos with pan-mesodermal loss of Fgf8 expression. Surprisingly, despite previous models in which Fgf8 has been assigned a pivotal role in segmentation/somite differentiation, Fgf8 is not required for these processes. However, mutant neonates display severe renal hypoplasia with deficient nephron formation. In mutant kidneys, aberrant cell death occurs within the metanephric mesenchyme (MM), particularly in the cortical nephrogenic zone, which provides the progenitors for recurring rounds of nephron formation. Prior to mutant morphological changes, Wnt4 and Lim1 expression, which is essential for nephrogenesis, is absent in MM. Furthermore, comparative analysis of Wnt4-null homozygotes reveals concomitant downregulation of Lim1 and diminished tubule formation. Our data support a model whereby FGF8 and WNT4 function in concert to induce the expression of Lim1 for MM survival and tubulogenesis

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External Sources

  1. View record in Web of Science®
  2. WOS: 000232430900007

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