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

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

Research output: Contribution to journalArticle

279 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)3105-3115
Number of pages11
JournalDevelopment
Volume128
Issue number16
StatePublished - 2001

Keywords

  • Kidney
  • Mouse
  • Sall1
  • Townes-Brocks syndrome

ASJC Scopus subject areas

  • Anatomy
  • Cell Biology

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