期刊
DEVELOPMENT
卷 138, 期 6, 页码 1161-1172出版社
COMPANY BIOLOGISTS LTD
DOI: 10.1242/dev.057620
关键词
Fz4; Fz8; Kidney development; Wnt11; Wnt signaling; Organ size control; Mouse
资金
- Howard Hughes Medical Institute
- National Eye Institute (NIH)
The developing mammalian kidney is an attractive system in which to study the control of organ growth. Targeted mutations in the Wnt receptors frizzled (Fz) 4 and Fz8 lead to reduced ureteric bud growth and a reduction in kidney size, a phenotype previously reported for loss of Wnt11. In cell culture, Fz4 and Fz8 can mediate noncanonical signaling stimulated by Wnt11, but only Fz4 mediates Wnt11-stimulated canonical signaling. In genetically mosaic mouse ureteric buds, competition between phenotypically mutant Fz4(-/-) or Fz4(-/-); Fz8(-/-) cells and adjacent phenotypically wild-type Fz4(+/-) or Fz4(+/-); Fz(8-/-) cells results in under-representation of the mutant cells to an extent far greater than would be predicted from the size reduction of homogeneously mutant kidneys. This discrepancy presumably reflects the compensatory action of a network of growth regulatory systems that minimize developmental perturbations. The present work represents the first description of a kidney phenotype referable to one or more Wnt receptors and demonstrates a general strategy for revealing the contribution of an individual growth regulatory pathway when it is part of a larger homeostatic network.
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