In:
Genes & Development, Cold Spring Harbor Laboratory, Vol. 11, No. 15 ( 1997-08-01), p. 1938-1948
Abstract:
Expression of AP-2 transcription factors has been detected previously in embryonic renal tissues. We show here that AP-2β −/− 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-2β-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-2β 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-2β gene is located in close proximity to but distinct from the ARPKD gene.
Type of Medium:
Online Resource
ISSN:
0890-9369
,
1549-5477
DOI:
10.1101/gad.11.15.1938
Language:
English
Publisher:
Cold Spring Harbor Laboratory
Publication Date:
1997
detail.hit.zdb_id:
1467414-2
SSG:
12
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