| First Author | Spence MJ | Year | 1995 |
| Journal | Somat Cell Mol Genet | Volume | 21 |
| Issue | 1 | Pages | 1-18 |
| PubMed ID | 7604355 | Mgi Jnum | J:26231 |
| Mgi Id | MGI:73895 | Doi | 10.1007/BF02255818 |
| Citation | Spence MJ, et al. (1995) Analysis of mutations in alleles of the fur gene from an endoprotease-deficient Chinese hamster ovary cell strain. Somat Cell Mol Genet 21(1):1-18 |
| abstractText | RPE.40 mutant cells differ from wild-type Chinese hamster ovary (CHO-K1) cells in their increased resistance to Pseudomonas exotoxin A and their inability to process the insulin proreceptor and certain viral envelope proproteins. Northern analysis revealed that RPE.40 cells maintained a substantially lower steady-state level of 4.0 kb fur mRNA than did CHO-K1 cells. Analysis of fur cDNAs showed that RPE.40 cells were diploid at the fur locus, and RPE.40 cells had a Cys (TGC) to Tyr (TAC) mutation in codon 196 of one allele (allele I). Approximately 25-30% of the CHO-K1 cells were also heterozygous (Tyr/Cys) at codon 196, and pre-mRNAs transcribed from the second allele (allele II) in RPE.40 cells were defectively spliced. All other pre-mRNAs were correctly spliced. Rapid turnover of defectively spliced transcripts may account for the reduced steady-state level of fur mRNA observed in RPE.40 cells. Our results provide a mechanistic basis for the endoprotease-deficient phenotype of RPE.40 cells. |
