The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 
 
 

Loss of Tbx4 blocks hindlimb development and affects vascularization and fusion of the allantois.

Tbx4 is a member of the T-box family of transcription factor genes, which have been shown to play important roles in development. We have ablated Tbx4 function using targeted mutagenesis in the mouse. Embryos homozygous for the null allele fail to undergo chorioallantoic fusion and die by 10.5 days post coitus. The allantoises of Tbx4-mutant embryos are stunted, apoptotic and display abnormal differentiation. Endothelial cells within mutant allantoises do not undergo vascular remodeling. Heterozygous embryos show a mild, transient growth defect in the allantois. Induction of a hindlimb field occurs normally in Tbx4 mutants and initial patterning of the hindlimb bud appears normal. However, hindlimb buds from Tbx4 mutants fail to develop either in vivo or in vitro and do not maintain Fgf10 expression in the mesenchyme. The expression of another, closely-linked, T-box gene, Tbx2, is reduced in both the hindlimb and the allantois of Tbx4-mutant embryos prior to the development of overt morphological abnormalities, which suggests that Tbx4 regulates Tbx2 in these tissues.[1]

References

 
WikiGenes - Universities