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Enhanced apoptotic cell death of renal epithelial cells in mice lacking transcription factor AP-2beta.

Expression of AP-2 transcription factors has been detected previously in embryonic renal tissues. We show here that AP-2beta -/- mice complete embryonic development and die at postnatal days 1 and 2 because of polycystic kidney disease. Analyses of kidney development revealed that induction of epithelial conversion, mesenchyme condensation, and further glomerular and tubular differentiation occur normally in AP-2beta-deficient mice. At the end of embryonic development expression of bcl-X(L), bcl-w, and bcl-2 is down-regulated in parallel to massive apoptotic death of collecting duct and distal tubular epithelia. Addressing the molecular mechanism we show that transfection of AP-2 into cell lines in vitro strongly suppresses c-myc-induced apoptosis pointing to a function of AP-2 in programming cell survival during embryogenesis. The position of the human AP-2beta gene was identified at chromosome 6p12-p21.1, within a region that has been mapped for autosomal recessive polycystic kidney disease (ARPKD). Sequence analyses of ARPKD patients and linkage analyses using intragenic polymorphic markers indicate that the AP-2beta gene is located in close proximity to but distinct from the ARPKD gene.

Pubmed ID: 9271117

Authors

  • Moser M
  • Pscherer A
  • Roth C
  • Becker J
  • Mücher G
  • Zerres K
  • Dixkens C
  • Weis J
  • Guay-Woodford L
  • Buettner R
  • Fässler R

Journal

Genes & development

Publication Data

August 1, 1997

Associated Grants

None

Mesh Terms

  • Animals
  • Apoptosis
  • Cells, Cultured
  • Chromosome Mapping
  • Chromosomes, Human, Pair 6
  • DNA-Binding Proteins
  • Embryonic and Fetal Development
  • Epithelial Cells
  • Gene Expression Regulation, Developmental
  • Genes, myc
  • Genetic Linkage
  • Humans
  • Kidney
  • Kidney Tubules
  • Mice
  • Mice, Knockout
  • Molecular Sequence Data
  • Phenotype
  • Polycystic Kidney, Autosomal Recessive
  • Restriction Mapping
  • Sequence Analysis, DNA
  • Transcription Factor AP-2
  • Transcription Factors