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      Kidney Development: An Overview

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          Abstract

          Background: Kidney diseases are worldwide public health problems with a high cost and increasing incidence. By revealing the genetic and cellular mechanism behind mammalian kidney development, better diagnostic methods and novel therapies can be expected to be developed. The mammalian kidney is a typical organ that develops on the basis of sequential and reciprocal cell and tissue interactions. Functional genetic analysis has identified that genes from different classes are involved in the construction of the kidney and the same genes are also connected to the development of diseases. Summary: This review gives an overview of the basics of kidney ontogeny, from identification of the primary kidney cell to inductive signals of ureter budding and formation of the segmented nephron. We also go through some of the key factors involved in the control of morphogenesis. Key Message: Despite the wealth of accumulated data on nephron development, including progenitor cell control factors and inductive signals, many of the detailed mechanisms remain to be revealed.

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          Most cited references19

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          Six2 defines and regulates a multipotent self-renewing nephron progenitor population throughout mammalian kidney development.

          Nephrons, the basic functional units of the kidney, are generated repetitively during kidney organogenesis from a mesenchymal progenitor population. Which cells within this pool give rise to nephrons and how multiple nephron lineages form during this protracted developmental process are unclear. We demonstrate that the Six2-expressing cap mesenchyme represents a multipotent nephron progenitor population. Six2-expressing cells give rise to all cell types of the main body of the nephron during all stages of nephrogenesis. Pulse labeling of Six2-expressing nephron progenitors at the onset of kidney development suggests that the Six2-expressing population is maintained by self-renewal. Clonal analysis indicates that at least some Six2-expressing cells are multipotent, contributing to multiple domains of the nephron. Furthermore, Six2 functions cell autonomously to maintain a progenitor cell status, as cap mesenchyme cells lacking Six2 activity contribute to ectopic nephron tubules, a mechanism dependent on a Wnt9b inductive signal. Taken together, our observations suggest that Six2 activity cell-autonomously regulates a multipotent nephron progenitor population.
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            Wnt9b plays a central role in the regulation of mesenchymal to epithelial transitions underlying organogenesis of the mammalian urogenital system.

            The vertebrate urogenital system forms due to inductive interactions between the Wolffian duct, its derivative the ureteric bud, and their adjacent mesenchymes. These establish epithelial primordia within the mesonephric (embryonic) and metanephric (adult) kidneys and the Müllerian duct, the anlage of much of the female reproductive tract. We show that Wnt9b is expressed in the inductive epithelia and is essential for the development of mesonephric and metanephric tubules and caudal extension of the Müllerian duct. Wnt9b is required for the earliest inductive response in metanephric mesenchyme. Further, Wnt9b-expressing cells can functionally substitute for the ureteric bud in these interactions. Wnt9b acts upstream of another Wnt, Wnt4, in this process, and our data implicate canonical Wnt signaling as one of the major pathways in the organization of the mammalian urogenital system. Together these findings suggest that Wnt9b is a common organizing signal regulating diverse components of the mammalian urogenital system.
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              Epithelial transformation of metanephric mesenchyme in the developing kidney regulated by Wnt-4.

              The kidney has been widely exploited as a model system for the study of tissue inductions regulating vertebrate organogenesis. Kidney development is initiated by the ingrowth of the Wolfian duct-derived ureteric bud into the presumptive kidney mesenchyme. In response to a signal from the ureter, mesenchymal cells condense, aggregate into pretubular clusters and undergo an epithelial conversion generating a simple tubule. This then undergoes morphogenesis and is transformed into the excretory system of the kidney, the nephron. We report here that the expression of Wnt-4, which encodes a secreted glycoprotein, correlates with, and is required for, kidney tubulogenesis. Mice lacking Wnt-4 activity fail to form pretubular cell aggregates; however, other aspects of mesenchymal and ureteric development are unaffected. Thus, Wnt-4 appears to act as an autoinducer of the mesenchyme to epithelial transition that underlies nephron development.
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                Author and article information

                Journal
                NEE
                Nephron Exp Nephrol
                10.1159/issn.1660-2129
                Cardiorenal Medicine
                S. Karger AG
                978-3-318-02677-1
                978-3-318-02678-8
                1660-2129
                2014
                May 2014
                19 May 2014
                : 126
                : 2
                : 40-44
                Affiliations
                Oulu Center for Cell-Matrix Research, Biocenter and Infotech Oulu, Laboratory of Developmental Biology, Intelligent Systems, Faculty of Biochemistry and Molecular Medicine, University of Oulu, Oulu, Finland
                Author notes
                *Prof. Seppo Vainio, Biocenter Oulu, Laboratory of Developmental Biology, University of Oulu, Aapistie 5, PO Box 5000, FI-90220 Oulu (Finland), E-Mail seppo.vainio@oulu.fi
                Article
                360659 Nephron Exp Nephrol 2014;126:40-44
                10.1159/000360659
                24854638
                e2f2da11-d965-4821-9120-6596f21cb1f9
                © 2014 S. Karger AG, Basel

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                History
                Page count
                Figures: 1, Pages: 5
                Categories
                Further Section

                Cardiovascular Medicine,Nephrology
                Embryonic induction,Branching,Developmental programming,Inductive tissue interactions,Inductive signaling,Nephrogenesis,Polarization,Mesenchyme-epithelium transition,Glomerulogenesis,Segmentation

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