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Am J Physiol Renal Physiol (May 9, 2007). doi:10.1152/ajprenal.00416.2006
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Submitted on October 20, 2006
Accepted on May 3, 2007

Canonical WNT signaling during kidney development

Diana Margarita Iglesias1, Pierre-Alain Hueber2, LeeLee Chu3, Robert Campbell3, Anne-Marie Patenaude3, Alison J. Dziarmaga1, Jacklyn Quinlan1, Othman Mohamed4, Daniel Dufort4, and Paul R. Goodyer3*

1 Human Genetics, McGill University, Montreal, Canada
2 Experimental Medicine, McGill University, Montreal, Canada
3 Pediatrics, McGill University, Montreal, Canada
4 Obstetrics and Gynecology, McGill University, Montreal, Canada

* To whom correspondence should be addressed. E-mail: paul.goodyer{at}mcgill.ca.

The canonical WNT signaling pathway plays a crucial role in patterning of the embryo during development, but little is known about the specific developmental events, which are under WNT control. To understand more about how the WNT pathway orchestrates mammalian organogenesis, we studied the canonical {beta}-catenin mediated WNT signaling pathway in kidneys of mice bearing a {beta}-catenin responsive TCF/{beta}Gal reporter transgene. In metanephric kidney, intense canonical WNT signaling was evident in epithelia of the branching ureteric bud and in nephrogenic mesenchyme during its transition into renal tubules. WNT signaling activity is rapidly downregulated in maturing nephrons and becomes undetectable in post-natal kidney. Sites of TCF/{beta}bGal activity are in proximity to the known sites of renal WNT2b and WNT4 expression, and these WNTs stimulate TCF reporter activity in kidney cell lines derived from ureteric bud and metanephric mesenchyme lineages. When fetal kidney explants from HoxB7/GFP mice were exposed to the canonical WNT signaling pathway inhibitor, Dickkopf-1, arborization of the ureteric bud was significantly reduced. We conclude that restricted zones of intense canonical WNT signaling drive branching nephrogenesis in fetal kidney.




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