||Do Trifluorothymidine-Resistant Mutants of L5178Y Mouse Lymphoma Cells Re-Express Thymidine Kinase Activity Following 5-Azacytidine Treatment (Journal Version).
Moore, M. M. ;
Applegate, M. L. ;
Hozier, J. C. ;
||Health Effects Research Lab., Research Triangle Park, NC. ;Florida Inst. of Tech., Melbourne.
Chromosome abnormalities ;
Azo compounds ;
Thymidine kinase ;
Gene expression ;
||Most EPA libraries have a fiche copy filed under the call number shown. Check with individual libraries about paper copy.
TFT is an effective selective agent for TK-deficient mutants of mouse lymphoma cells. Mutants can be classified by colony size into small colonies (many of which show readily observable chromosome abnormalities associated with chromosome 11-the location of the TK gene) and large colonies (which may represent events affecting only the expression of the TK gene). The hypomethylating agent 5-azacyidine can be utilized to investigate the possibility that mutants might be the result of a suppressed rather than an altered TK gene. Some of the mutants may be TK deficient due to the translocation of the TK gene into a chromosomal environment precluding the expression (position effect) rather than actual damage at the TK locus. One mechanism for gene inactivation due to position effect might be transfer of the gene to a region of the chromosome where the DNA is highly methylated, a condition known to be associated with inactivation of some genes. In the studies, 11 mutants have been evaluated. None of the 11, including 10 small-colony mutants (6 with chromosome 11 translocations) and 1 large-colony mutant, show a high conversion to TK competency following 5-azacytidine treatment. (Copyright (c) 1988 Elsevier Science Publishers B.V.)