The TWis gene product is altered, but the TWis/TWis phenotype is very similar to that of T/T embryos which lack T. In early TWis/TWis embryos T expression is normal, but ceases prematurely during early organogenesis coincident with a cessation of mesoderm formation. The archenteron/node region is disrupted and the extension of the notochord precursor comes to a halt, followed by a decrease and finally a complete loss of T gene expression in the primitive streak and the head process/notochord precursor. It appears that the primary defect of the mutant embryo is the disruption of the notochord precursor in the node region, which is required for axis elongation. Thus the T gene product is directly or indirectly involved in the organization of axial development. (Herrmann BG, 1991, Development 113 (3) 913-7)
The Twis mutation arose spontaneously on a strain A/J chromosome in the congenic line 129.A in the laboratory of Alexandra Shedlovsky, Thomas R. King, and William F. Dove at the McArdle Laboratory for Cancer Research and Laboratory of Genetics, University of Wisconsin.
|Allele Name||brachyury Wisconsin|
|Gene Symbol and Name||T, brachyury, T-box transcription factor T|
|Strain of Origin||A/J|
|Molecular Note||Restriction mapping showed that this allele comprises a 5.5 kb early transposon-like insertion element. RT-PCR based analysis shows that at least 8 different mutant transcripts are produced from the TWis allele. These transcripts bypass the mutated exon 7 splice donor site and no wild-type T transcripts are produced.|