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Insertion mutagenesis of embryonal carcinoma cells by retroviruses
Science (New York, N.Y.)
|May 3, 1985
Abstract:
Mutagenesis was studied in cultured F9 embryonal carcinoma cells infected with a variant of Moloney murine leukemia virus. Proviral insertion induced the inactivation of the hypoxanthine phosphoribosyltransferase locus, and the virus was used to isolate the mutated genes rapidly. Mutagenesis by these methods may be useful for the genetic dissection of the various mammalian cell phenotypes.
Insights
Moloney murine leukemia virus mutagenesis inactivated the hypoxanthine phosphoribosyltransferase gene in F9 cells. This viral mutagenesis method enables rapid isolation of mutated genes for cell phenotype studies.
Area of Science:
- Molecular Biology
- Genetics
- Virology
Background:
- Cultured F9 embryonal carcinoma cells are a model for studying mammalian development and gene function.
- Murine leukemia viruses are known to cause mutations through proviral insertion.
Purpose of the Study:
- To investigate mutagenesis in F9 cells using a Moloney murine leukemia virus variant.
- To develop a method for rapid isolation of mutated genes.
Main Methods:
- Infection of F9 embryonal carcinoma cells with a Moloney murine leukemia virus variant.
- Selection and isolation of cells with inactivated hypoxanthine phosphoribosyltransferase (HPRT) locus.
Main Results:
- Proviral insertion of the virus led to the inactivation of the HPRT locus.
- The virus facilitated the rapid isolation of genes mutated by proviral insertion.
Conclusions:
- This viral mutagenesis approach is effective for gene inactivation in F9 cells.
- The method holds potential for the genetic dissection of mammalian cell phenotypes.