thymidine-5--triphosphate and Sex-Chromosome-Aberrations

thymidine-5--triphosphate has been researched along with Sex-Chromosome-Aberrations* in 2 studies

Other Studies

2 other study(ies) available for thymidine-5--triphosphate and Sex-Chromosome-Aberrations

Article	Year
Fragile X expression in thymidine-prototrophic and auxotrophic human-mouse somatic cell hybrids under low and high thymidylate stress conditions. Cytogenetics and cell genetics, 1988, Volume: 47, Issue:4 Expression of the fragile X site fra(X)(q27.3) was studied in thymidine-prototrophic and auxotrophic human-mouse somatic cell hybrids. In these cells, low thymidylate stress, achieved by 5-fluoro-2'-deoxyuridine (FdU) treatment and by limiting the exogenous supply of thymidine (dT), induced fragile X expression. High thymidylate stress, produced by supplying excess amounts of dT, was also effective in inducing fragile X expression, even in a hybrid clone that retained a fragile X chromosome as the only human chromosome; addition of deoxycytidine (dC) completely abolished this effect. In contrast, 5-bromo-2'-deoxyuridine (BrdU) did not induce fragile X expression. Cell-cycle analysis of BrdU-deprived thymidine-auxotrophic hybrid cells indicated that one round of DNA replication under thymidylate stress conditions is sufficient for fragile X expression. Our results suggest that the expression is an intrinsic property of the fragile site itself, which is believed to be composed of replicon clusters with pyrimidine-rich DNA sequence(s). Topics: Animals; Bromodeoxyuridine; Cell Cycle; Deoxycytosine Nucleotides; Fragile X Syndrome; Gene Expression Regulation; Humans; Hybrid Cells; Male; Mice; Multigene Family; Replicon; Sex Chromosome Aberrations; Thymidine; Thymidine Monophosphate; Thymine Nucleotides	1988
Thymidylate metabolism in fragile X syndrome cells. Somatic cell and molecular genetics, 1985, Volume: 11, Issue:4 The observation that decreased thymidylate supply in vitro induces the expression of the Xq27 chromosome fragile site prompted us to examine cellular thymidylate metabolism. Using a sensitive enzyme assay for deoxyribonucleotide triphosphates, we found that the total cellular thymidine triphosphate pools in cell lines from fragile X patients and carriers do not differ from normal controls under either basal or folate-deficient conditions. This agrees with our earlier observation that the thymidylate synthase enzyme activities in crude cell extracts of five fragile X syndrome lymphoblast lines do not differ from those in normal controls under standard assay conditions. Although a difference in the amount of thymidine triphosphate available at the replication fork for DNA synthesis remains a possibility, our results indicate that a readily demonstrable defect in thymidylate metabolism is not present in fragile X syndrome cells. Topics: Aneuploidy; Cell Line; Deoxyribonucleotides; Female; Folic Acid; Folic Acid Antagonists; Fragile X Syndrome; Heterozygote; Humans; Lymphocytes; Male; Ribonucleotide Reductases; Sex Chromosome Aberrations; Thymidine Monophosphate; Thymidylate Synthase; Thymine Nucleotides	1985

Article

Year

Fragile X expression in thymidine-prototrophic and auxotrophic human-mouse somatic cell hybrids under low and high thymidylate stress conditions.

Cytogenetics and cell genetics, 1988, Volume: 47, Issue:4

Expression of the fragile X site fra(X)(q27.3) was studied in thymidine-prototrophic and auxotrophic human-mouse somatic cell hybrids. In these cells, low thymidylate stress, achieved by 5-fluoro-2'-deoxyuridine (FdU) treatment and by limiting the exogenous supply of thymidine (dT), induced fragile X expression. High thymidylate stress, produced by supplying excess amounts of dT, was also effective in inducing fragile X expression, even in a hybrid clone that retained a fragile X chromosome as the only human chromosome; addition of deoxycytidine (dC) completely abolished this effect. In contrast, 5-bromo-2'-deoxyuridine (BrdU) did not induce fragile X expression. Cell-cycle analysis of BrdU-deprived thymidine-auxotrophic hybrid cells indicated that one round of DNA replication under thymidylate stress conditions is sufficient for fragile X expression. Our results suggest that the expression is an intrinsic property of the fragile site itself, which is believed to be composed of replicon clusters with pyrimidine-rich DNA sequence(s).

Topics: Animals; Bromodeoxyuridine; Cell Cycle; Deoxycytosine Nucleotides; Fragile X Syndrome; Gene Expression Regulation; Humans; Hybrid Cells; Male; Mice; Multigene Family; Replicon; Sex Chromosome Aberrations; Thymidine; Thymidine Monophosphate; Thymine Nucleotides

1988

Thymidylate metabolism in fragile X syndrome cells.

Somatic cell and molecular genetics, 1985, Volume: 11, Issue:4

The observation that decreased thymidylate supply in vitro induces the expression of the Xq27 chromosome fragile site prompted us to examine cellular thymidylate metabolism. Using a sensitive enzyme assay for deoxyribonucleotide triphosphates, we found that the total cellular thymidine triphosphate pools in cell lines from fragile X patients and carriers do not differ from normal controls under either basal or folate-deficient conditions. This agrees with our earlier observation that the thymidylate synthase enzyme activities in crude cell extracts of five fragile X syndrome lymphoblast lines do not differ from those in normal controls under standard assay conditions. Although a difference in the amount of thymidine triphosphate available at the replication fork for DNA synthesis remains a possibility, our results indicate that a readily demonstrable defect in thymidylate metabolism is not present in fragile X syndrome cells.

Topics: Aneuploidy; Cell Line; Deoxyribonucleotides; Female; Folic Acid; Folic Acid Antagonists; Fragile X Syndrome; Heterozygote; Humans; Lymphocytes; Male; Ribonucleotide Reductases; Sex Chromosome Aberrations; Thymidine Monophosphate; Thymidylate Synthase; Thymine Nucleotides

1985