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Murine homolog of SALL1 is essential for ureteric bud invasion in kidney development

  1. Author:
    Nishinakamura, R.
    Matsumoto, Y.
    Nakao, K.
    Nakamura, K.
    Sato, A.
    Copeland, N. G.
    Gilbert, D. J.
    Jenkins, N. A.
    Scully, S.
    Lacey, D. L.
    Katsuki, M.
    Asashima, M.
    Yokota, T.

  2. Author Address

    Univ Tokyo, Inst Med Sci, Div Stem Cell Regulat, 4-6-1 Shirokanedai, Tokyo 1088639, Japan. Univ Tokyo, Inst Med Sci, Div Stem Cell Regulat, Tokyo 1088639, Japan. Univ Tokyo, Inst Med Sci, Lab DNA Biol & Embryo Engn, Tokyo 1088639, Japan. Univ Tokyo, Dept Life Sci, Tokyo 1538902, Japan. Natl Canc Inst, Mouse Canc Genet Program, Frederick, MD 21702 USA. Amgen Inc, Dept Pathol, Thousand Oaks, CA 91320 USA. Nishinakamura R Univ Tokyo, Inst Med Sci, Div Stem Cell Regulat, 4-6-1 Shirokanedai, Tokyo 1088639, Japan.
    1. Year: 2001
  2. Journal: Development
    1. 128
    2. 16
    3. Pages: 3105-3115
  4. Type of Article: Article
  1. Abstract:

    SALL1 is a mammalian homolog of the Drosophila region-specific homeotic gene spalt (sal); heterozygous mutations in SALL1 in humans lead to Townes-Brocks syndrome. We have isolated a mouse homolog of SALL1 (Sall1) and found that mice deficient in Sall1 die in the perinatal period and that kidney agenesis or severe dysgenesis are present. Sall1 is expressed in the metanephric mesenchyme surrounding ureteric bud; homozygous deletion of Sall1 results in an incomplete ureteric bud outgrowth, a failure of tubule formation in the mesenchyme and an apoptosis of the mesenchyme. This phenotype is likely to be primarily caused by the absence of the inductive signal from the ureter, as the Sall1-deficient mesenchyme is competent with respect to epithelial. differentiation. Sall1 is therefore essential for ureteric bud invasion, the initial key step for metanephros development.

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