|Presenting Author(s)||Przemko Tylzanowski|
|Abstract Title||Characterization of the noggin null phenotype in CD1 mouse genetic background.|
|Full author List||Liese Mebis, Przemko Tylzanowski, Kristof Van den Bergh and Frank Luyten.|
|Text of abstract||
Noggin is a secreted peptide that binds and inactivates BMPs, members of the transforming growth factor beta superfamily of secreted signaling molecules. In vertebrate limbs, Noggin is expressed in condensing cartilage and immature chondrocytes. Inactivation of the Noggin gene was initially carried out in an inbred 129SvJ mouse genetic background (Brunet et al , Nature, 1998) and subsequently outcrossed into the C57Bl6 mouse strain (McMahon et al ., Genes and Development, 1998). The null allele was lethal at birth and resulted in severe hyperplasia of the cartilage together with multiple joint fusions. Maturation of the cartilage, however, appeared to be normal.
In order to investigate the effect of the genetic background on the phenotypic manifestation of noggin inactivation, we have crossed the noggin null allele into the CD1 outbred and DBA1 inbred mouse strains. Additionally, we have further analyzed this mutation in C57Bl6 mouse background.
The phenotypic consequences of noggin inactivation in CD1 and Dba1 mouse strains were similar while the C57/Bl6 genetic background induced a markedly different phenotype. A number of differences among the mouse strains was identified in the skeletal development, including that of the limb. To further characterize the consequences of noggin inactivation on limb development, histological and gene marker analysis was carried out on 12.5, 13.5, 14.5 dpc and newborn limbs. The results of this work will be shown on the conference.
|Which session is your work most relevant to:||Limb patterning, Tissue differentiation.|
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