Mapping of recombinant retrovirus integration sites that cause expression of the viral genome in murine embryonal carcinoma cells.
Murine embryonal carcinoma (EC) cells do not normally express Moloney murine leukemia virus genes. Earlier, rare EC cell lines were isolated that expressed proviral neomycin resistance (neo) gene. This expression was dependent on cellular enhancer or promoter sequences that flank the proviral integration site. Four such integration sites, designated as Mint (for Moloney murine leukemia virus integration and expression sites in EC cells), have been mapped on mouse chromosomes. Minta, Mintb, Mintc and Mintd are unlinked and mapped on different chromosomes (Chr), Chr 10, Chr 1, Chr 5 and the X Chr, respectively. None of these loci appear to be linked to any known Mo-MuLV proviral integration sites previously mapped. These enhancer and promoter loci may represent a new set of genes active in undifferentiated embryonic cells.
Taketo
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M
Department of Microbiology and Immunology, Duke University Medical Center, Durham, North Carolina 27710.
Howard
T A
TA
Seldin
M F
MF
D000818:Animals; D015139:Blotting, Southern; D054278:Embryonal Carcinoma Stem Cells; D004742:Enhancer Elements, Genetic; D015967:Gene Expression Regulation, Viral; D005814:Genes, Viral; D051379:Mice; D008979:Moloney murine leukemia virus / Q000235:genetics*; D014411:Neoplastic Stem Cells; D011401:Promoter Regions, Genetic; D015183:Restriction Mapping; D016662:Virus Integration / Q000235:genetics*