Journal of the American Society of Nephrology
2007 JASN IMPACT FACTOR 7.111 HOME   AUTHOR INFO   EDITORIAL BOARD   SUBSCRIBE   FEEDBACK   ALERTS   HELP 
    advanced
CURRENT ISSUE ARCHIVES JASN Express ONLINE SUBMISSION


Published ahead of print on February 21, 2007
J Am Soc Nephrol 18: 1121-1129, 2007
© 2007 American Society of Nephrology
doi: 10.1681/ASN.2006070739
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
ASN.2006070739v1
18/4/1121    most recent
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Narlis, M.
Right arrow Articles by Bouchard, M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Narlis, M.
Right arrow Articles by Bouchard, M.

Genetics and Development

Pax2 and Pax8 Regulate Branching Morphogenesis and Nephron Differentiation in the Developing Kidney

Melina Narlis, David Grote, Yaned Gaitan, Sami K. Boualia and Maxime Bouchard

McGill Cancer Centre and Biochemistry Department, McGill University, Montreal, Quebec, Canada

Address correspondence to: Dr. Maxime Bouchard, McGill Cancer Centre and Biochemistry Department, McGill University, 3655 Promenade Sir-William-Osler, Montreal, Quebec H3G 1Y6, Canada. Phone: 514-398-3532; Fax: 514-398-6769; E-mail: maxime.bouchard{at}mcgill.ca

Received for publication July 14, 2006. Accepted for publication January 5, 2007.

Pax genes are important regulators of kidney development. In the mouse, homozygous Pax2 inactivation results in renal agenesis, a phenotype that has largely precluded the analysis of Pax gene function during metanephric kidney development. To address this later function, kidney development was analyzed in embryos that were compound heterozygous for Pax2 and for Pax8, a closely related member of the Pax gene family. Both genes are coexpressed in differentiating nephrons and collecting ducts. At the morphological level, Pax2+/–Pax8+/– metanephric kidneys are severely hypodysplastic and characterized by a reduction in ureter tips and nephron number in comparison with wild-type or Pax2+/– kidneys. In developing nephrons, the molecular analysis of Pax2+/–Pax8+/– kidneys reveals a strong reduction in the expression levels of Lim1, a key regulator of nephron differentiation, accompanied by an increase in apoptosis. At a more mature stage, the reduction of Pax2/8 gene dosage severely affects distal tubule formation, revealing a role for Pax genes in the differentiation of specific nephron segments. At the ureter tips, the expression of Wnt11, a target of glial cell–derived neurotrophic factor–Ret signaling, is significantly reduced, whereas the expression levels of Ret and GDNF remain normal. Together, these results demonstrate a crucial role for Pax2 and Pax8 in nephron differentiation and branching morphogenesis of the metanephros.




This article has been cited by other articles:


Home page
 J. Am. Soc. Nephrol.Home page
S. Hartwig, D. Bridgewater, V. Di Giovanni, J. Cain, Y. Mishina, and N. D. Rosenblum
BMP Receptor ALK3 Controls Collecting System Development
J. Am. Soc. Nephrol., January 1, 2008; 19(1): 117 - 124.
[Abstract] [Full Text] [PDF]


HOME CURRENT ISSUE ARCHIVES JASN Express ONLINE SUBMISSION AUTHOR INFO
EDITORIAL BOARD SUBSCRIBE FEEDBACK ALERTS HELP

Copyright © 2008 by the American Society of Nephrology. Online ISSN: 1533-3450 Print ISSN: 1046-6673