| First Author | Silver L | Year | 1979 |
| Journal | Mouse News Lett | Volume | 61 |
| Pages | 63 | Mgi Jnum | J:13823 |
| Mgi Id | MGI:62002 | Citation | Silver L, et al. (1979) The p63 gene. Mouse News Lett 61:63 |
| abstractText | Full text of MNL contribution: The p63 gene. The technique of two-dimensional gel electrophoresis was used to identify a major testicular cell protein, p63/6.9, which is specified by a gene (p63) within the mouse T/t-complex on chromosome 17 (Silver et al., 1979, Cell 17: 275-284). A wild-type gene causes the expression of one form of this protein, p63/6.9b. All lethal and semi-lethal t-haplotypes derived from wild mice cause the expression of an apparently identical alternate allelic form of the p63/6.9 protein. This protein, p63/6.9a, represents the first t-haplotype- specific molecule to be biochemically identified. A dominant haplotype (THp) acts as a null allele of the p63 gene; this unique behavior provides additional evidence for the interpretation of THp as a deletion within the T/t region of chromosome 17. Limited proteolysis of viable testicular cells causes selective cleavage of the p63/6.9 proteins, relative to other detergent-soluble testicular cell proteins known to be internal. This result strongly suggests that p63/6.9 proteins are located on the cell surface. Quantitative estimates indicate that p63/6.9 is one of the most prominent proteins on the testicular cell surface. p63/6.9 is expressed in all other mouse cell types analyzed but at much reduced levels. Partial t-haplotypes, obtained from infrequent recombination events, were used to map the p63 gene close to the dominant mutation T and separate from the lethal factors of t-haplotypes. A 100% correlation was observed between the expression of p63/6.9a and the genetic presence of the tail interaction factor of t-haplotypes. Seven independently derived dominant T mutations were analyzed for expression of the p63 gene. Two of these mutations (T40r and Tc) were radiation-induced and are presumably deletions over the +T gene. Chromosomes carrying these mutations or other T mutations expressed the wild-type allele of the p63 gene. Hence, the p63 gene is separate from the gene defined by T mutations. A possible interpretation of these results is that the p63 gene is equivalent to the tail interaction factor which therefore must also be separate from the T gene. The fact that recombination between T and the tail interaction factor has never been observed may be entirely a consequence of the suppression of recombination caused by the presence of t-haplotypes. We have found two chromosomes (Torl and tae5) in which expression of the p63 gene is anomalous. In both cases, a single chromosome expresses both forms of the p63/6.9 protein. At present, our only explanation is that both chromosomes were derived by unequal crossing over events in mice which were heterozygous for a t-haplotype. According to Dr. Salome Waelsch, this is a real possibility in the case of tae5. If anyone has information regarding the existence of t-haplotypes within the noninbred Swiss stock from which TOrl was derived (Mouse News Letter 48: 38), it would be greatly appreciated. (Silver, Kintanar) |
