Mouse teratocarcinoma mutant clones deficient in adenine phosphoribosyltransferase and developmentally pluripotent.
Mouse teratocarcinoma stem cells deficient in activity of adenine phosphoribosyltransferase (APRT; EC 2.4.2.7) were obtained in order to have this marker in developmentally versatile cells. Mutagenized stem-cell cultures were selected for resistance to 8-azaadenine and four clonal cell lines were isolated. Three had severe deficiencies of APRT activity (7% or less of wild type) and one had a moderate reduction (73%). The enzyme in the latter clone was found to be an electrophoretic variant with slightly less anodal migration than the wild-type enzyme. Each clone remained stably APRT-deficient for at least 3 1/2 weeks, after subcutaneous inoculation, in the absence of the selective agent. The tumors formed from the inocula comprised a variety of differentiated tissues and thus showed persistence of stem-cell developmental pluripotency despite mutagenesis and selection. All mutants also retained the quasinormal karyotype (X/O sex chromosomal constitution, trisomy-19) of the parent line. These lines are appropriate for such uses as production (by blastocyst injection) of mouse models of the human genetic deficiency and for foreign-gene transfer, via teratocarcinoma cells, into mice.
D000228:Adenine Phosphoribosyltransferase / Q000235:genetics / Q000378:metabolism*; D000818:Animals; D002999:Clone Cells; D005819:Genetic Markers; D014644:Genetic Variation; D051379:Mice; D009374:Neoplasms, Experimental / Q000201:enzymology; D010430:Pentosyltransferases / Q000378:metabolism*; D010641:Phenotype; D013724:Teratoma / Q000201:enzymology*
D005819:Genetic Markers; D010430:Pentosyltransferases; D000228:Adenine Phosphoribosyltransferase