Azacytidine induces reversion of thymidine kinase deficiency in Friend erythroleukemia cells.
Cells of the Friend erythroleukemia cell line show a high frequency of variants which have lost thymidine kinase activity. We have exposed a thymidine kinase-deficient clone of this cell line to a series of concentrations of azacytidine and found a dose-dependent induction of thymidine kinase-positive revertants. Maximum reversion occurred with 0.9 micrograms/ml azacytidine where the frequency of revertants amongst survivors was increased by a factor of 10(6) compared to that of control cultures. Revertants were found to have varying levels of thymidine kinase activity. We conclude that DNA methylation of one or both alleles of the thymidine kinase gene is largely responsible for the instability of this gene in Friend erythroleukemia cells.
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Hickey
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Jones
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O'Neill
D000483:Alleles; D000818:Animals; D001374:Azacitidine / Q000494:pharmacology*; D002460:Cell Line; D002999:Clone Cells; D004247:DNA / Q000378:metabolism*; D004305:Dose-Response Relationship, Drug; D005622:Friend murine leukemia virus; D005786:Gene Expression Regulation; D004915:Leukemia, Erythroblastic, Acute; D008745:Methylation; D051379:Mice; D013937:Thymidine Kinase / Q000096:biosynthesis* / Q000235:genetics
D004247:DNA; D013937:Thymidine Kinase; D001374:Azacitidine