Talk:Developmental Signals - Wnt: Difference between revisions

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==References==
==References==
Wnt1 signaling has been implicated as one factor involved in neural crest-derived melanocyte (NC-M) development. http://www.ncbi.nlm.nih.gov/pubmed/10963668
Proc Natl Acad Sci U S A. 2000 Aug 29;97(18):10050-5.
Neural crest-directed gene transfer demonstrates Wnt1 role in melanocyte expansion and differentiation during mouse development.
Dunn KJ, Williams BO, Li Y, Pavan WJ.
Genetic Disease Research Branch, National Human Genome Research Institute, and Division of Basic Sciences, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892-4472, USA.
Abstract
Wnt1 signaling has been implicated as one factor involved in neural crest-derived melanocyte (NC-M) development. Mice deficient for both Wnt1 and Wnt3a have a marked deficiency in trunk neural crest derivatives including NC-Ms. We have used cell lineage-directed gene targeting of Wnt signaling genes to examine the effects of Wnt signaling in mouse neural crest development. Gene expression was directed to cell lineages by infection with subgroup A avian leukosis virus vectors in lines of transgenic mice that express the retrovirus receptor tv-a. Transgenic mice with tva in either nestin-expressing neural precursor cells (line Ntva) or dopachrome tautomerase (DCT)-expressing melanoblasts (line DCTtva) were analyzed. We overstimulated Wnt signaling in two ways: directed gene transfer of Wnt1 to Ntva(+) cells and transfer of beta-catenin to DCTtva(+) NC-M precursor cells. In both methods, NC-M expansion and differentiation were effected. Significant increases were observed in the number of NC-Ms [melanin(+) and tyrosinase-related protein 1 (TYRP1)(+) cells], the differentiation of melanin(-) TYRP1(+) cells to melanin(+) TYRP1(+) NC-Ms, and the intensity of pigmentation per NC-M. These data are consistent with Wnt1 signaling being involved in both expansion and differentiation of migrating NC-Ms in the developing mouse embryo. The use of lineage-directed gene targeting will allow the dissection of signaling molecules involved in NC development and is adaptable to other mammalian developmental systems.


Endothelial specific stabilization of Wnt/beta-catenin signaling alters early vascular development in the embryo by upregulating Dll4/Notch signaling (Dev Cell, June 2010).
Endothelial specific stabilization of Wnt/beta-catenin signaling alters early vascular development in the embryo by upregulating Dll4/Notch signaling (Dev Cell, June 2010).

Revision as of 19:20, 30 September 2010

References

Wnt1 signaling has been implicated as one factor involved in neural crest-derived melanocyte (NC-M) development. http://www.ncbi.nlm.nih.gov/pubmed/10963668

Proc Natl Acad Sci U S A. 2000 Aug 29;97(18):10050-5. Neural crest-directed gene transfer demonstrates Wnt1 role in melanocyte expansion and differentiation during mouse development. Dunn KJ, Williams BO, Li Y, Pavan WJ.

Genetic Disease Research Branch, National Human Genome Research Institute, and Division of Basic Sciences, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892-4472, USA. Abstract Wnt1 signaling has been implicated as one factor involved in neural crest-derived melanocyte (NC-M) development. Mice deficient for both Wnt1 and Wnt3a have a marked deficiency in trunk neural crest derivatives including NC-Ms. We have used cell lineage-directed gene targeting of Wnt signaling genes to examine the effects of Wnt signaling in mouse neural crest development. Gene expression was directed to cell lineages by infection with subgroup A avian leukosis virus vectors in lines of transgenic mice that express the retrovirus receptor tv-a. Transgenic mice with tva in either nestin-expressing neural precursor cells (line Ntva) or dopachrome tautomerase (DCT)-expressing melanoblasts (line DCTtva) were analyzed. We overstimulated Wnt signaling in two ways: directed gene transfer of Wnt1 to Ntva(+) cells and transfer of beta-catenin to DCTtva(+) NC-M precursor cells. In both methods, NC-M expansion and differentiation were effected. Significant increases were observed in the number of NC-Ms [melanin(+) and tyrosinase-related protein 1 (TYRP1)(+) cells], the differentiation of melanin(-) TYRP1(+) cells to melanin(+) TYRP1(+) NC-Ms, and the intensity of pigmentation per NC-M. These data are consistent with Wnt1 signaling being involved in both expansion and differentiation of migrating NC-Ms in the developing mouse embryo. The use of lineage-directed gene targeting will allow the dissection of signaling molecules involved in NC development and is adaptable to other mammalian developmental systems.


Endothelial specific stabilization of Wnt/beta-catenin signaling alters early vascular development in the embryo by upregulating Dll4/Notch signaling (Dev Cell, June 2010).

Wnt3a deficiency irreversibly impairs hematopoietic stem cell self-renewal and leads to defects in progenitor cell differentiation (Blood, Jan 2009).

The nuclear import of Frizzled2-C by Importins-beta11 and alpha2 promotes postsynaptic development. Therefore, Wnt-activated growth of the post-synaptic membrane is mediated by the synapse-to-nucleus translocation and active nuclear import of Fz2-C (Nat Neurosci, August 2010).