|
|
Blood, 1 January 2008, Vol. 111, No. 1, pp. 160-164.
Prepublished online as a Blood First Edition Paper on September 13, 2007; DOI 10.1182/blood-2007-07-099754.
 Previous Article | Next Article 
Submitted July 16, 2007
Accepted August 25, 2007
Simultaneous loss of  - and  -catenin does not perturb hematopoiesis or lymphopoiesis
Ute Koch, Anne Wilson, Monica Cobas, Rolf Kemler, H. Robson MacDonald, and Freddy Radtke*
Swiss Institute for Experimental Cancer Research (ISREC), Ecole Polytechnique Federale de Lausanne (EPFL), Epalinges, Vaud, Switzerland
Ludwig Institute for Cancer Research, Lausanne Branch, University of Lausanne, Epalinges, Vaud, Switzerland
Department of Molecular Embryology, Max-Planck Institute of Immunology, Freiburg, Germany
* Corresponding author; email: freddy.radtke{at}isrec.ch.
Hematopietic stem cells (HSC) maintain life-long hematopoiesis in the bone marrow via their ability to self-renew and to differentiate into all blood lineages. Although a central role for the canonical wnt signaling pathway has been suggested in HSC self-renewal as well as in the development of B and T cells, conditional deletion of  -catenin (which is considered to be essential for wnt signaling) has no effect on hematopoiesis or lymphopoiesis. Here we address whether this discrepancy can be explained by a redundant and compensatory function of  -catenin, a close homologue of -catenin. Unexpectedly, we find that combined deficiency of - and -catenin in hematopoietic progenitors does not impair their ability to self-renew and to reconstitute all myeloid, erythroid and lymphoid lineages, even in competitive mixed chimeras and serial transplants. These results exclude an essential role for canonical wnt signaling (as mediated by - and/or -catenin) during hematopoiesis and lymphopoiesis.
 CiteULike  Connotea  Del.icio.us  Digg  Reddit  Technorati What's this?
This article has been cited by other articles:
|
|
|
|
 
M. Xu, A. Sharma, D. L. Wiest, and J. M. Sen
Pre-TCR-Induced {beta}-Catenin Facilitates Traversal through {beta}-Selection
J. Immunol.,
January 15, 2009;
182(2):
751 - 758.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
T. C. Luis, F. Weerkamp, B. A. E. Naber, M. R. M. Baert, E. F. E. de Haas, T. Nikolic, S. Heuvelmans, R. R. De Krijger, J. J. M. van Dongen, and F. J. T. Staal
Wnt3a deficiency irreversibly impairs hematopoietic stem cell self-renewal and leads to defects in progenitor cell differentiation
Blood,
January 15, 2009;
113(3):
546 - 554.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
T. Yokota, K. Oritani, K. P. Garrett, T. Kouro, M. Nishida, I. Takahashi, M. Ichii, Y. Satoh, P. W. Kincade, and Y. Kanakura
Soluble Frizzled-Related Protein 1 Is Estrogen Inducible in Bone Marrow Stromal Cells and Suppresses the Earliest Events in Lymphopoiesis
J. Immunol.,
November 1, 2008;
181(9):
6061 - 6072.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
Q. Yu, W. J. Quinn III, T. Salay, J. E. Crowley, M. P. Cancro, and J. M. Sen
Role of {beta}-Catenin in B Cell Development and Function
J. Immunol.,
September 15, 2008;
181(6):
3777 - 3783.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
S. Malhotra, Y. Baba, K. P. Garrett, F. J. T. Staal, R. Gerstein, and P. W. Kincade
Contrasting Responses of Lymphoid Progenitors to Canonical and Noncanonical Wnt Signals
J. Immunol.,
September 15, 2008;
181(6):
3955 - 3964.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
T. Grigoryan, P. Wend, A. Klaus, and W. Birchmeier
Deciphering the function of canonical Wnt signals in development and disease: conditional loss- and gain-of-function mutations of {beta}-catenin in mice
Genes & Dev.,
September 1, 2008;
22(17):
2308 - 2341.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
