| First Author | Clark LS | Year | 2004 |
| Journal | Mutagenesis | Volume | 19 |
| Issue | 4 | Pages | 263-8 |
| PubMed ID | 15215324 | Mgi Jnum | J:91060 |
| Mgi Id | MGI:3045873 | Doi | 10.1093/mutage/geh024 |
| Citation | Clark LS, et al. (2004) Loss of P53 heterozygosity is not responsible for the small colony thymidine kinase mutant phenotype in L5178Y mouse lymphoma cells. Mutagenesis 19(4):263-268 |
| abstractText | The mouse lymphoma L5178Y Tk(+/-) 3.7.2C assay is a well-characterized in vitro system used for the study of somatic cell mutation. It was determined that this cell line has a heterozygous mutation in exon 5 of Trp53. Based on this assumption that the cell line is heterozygous for the Trp53 gene, it was postulated that the small colony thymidine kinase (Tk) mutant phenotype may be due to a newly induced mutation/deletion in both the Trp53 and Tk1 alleles. The resultant Tk(-/-) mutants would also be Trp53(+/0) or Trp53(+/+) and would lose their ability to grow at normal rates. Subsequently, we published our evaluation of the Trp53 status in L5178Y cells. This analysis included sequencing of Trp53 exon 4 and determined that the mouse lymphoma cell line has a mutation in both of the Trp53 alleles and, therefore, no wild-type Trp53 allele in either Tk(+/-) cells or Tk(-/-) mutants. Because the cells have no wild-type Trp53, it is not possible that the small colony phenotype results from a newly induced loss of both functional Trp53 and Tk. To determine whether small colonies might, however, include the deletion of both Trp53 and Tk we evaluated, using microsatellite marker analysis, a series of small colony mutants. We also utilized in situ hybridization to determine that the Trp53 alleles are, in fact, in their normal chromosome 11 location in Tk(+/-) 3.7.2C mouse lymphoma cells. From all of these analyses we can conclude that the small colony mutant phenotype is not caused by deletion of both Trp53 and Tk1. |
