Adenosine kinase deficiency in tritiated deoxyadenosine-resistant mouse S49 lymphoma cell lines

K. Jagannadha Sastry, Cecilia Huang, Teh sheng Chan

Research output: Contribution to journalArticlepeer-review

3 Scopus citations

Abstract

Mutant sublines were derived of S49 mouse T-lymphoma cells that were resistant to tritiated deoxyadenosine. Twenty-five isolates that were selected in 1 μCi/ml of the nucleoside were cross-resistant to 6-thioguanine, were sensitive to HAT (hypoxanthine, aminopterin, and thymidine), and contained less than 1% of hypoxanthine phosphoribosyltransferase activity in wildtype cells. One of the mutant clones, S49-dA2, was further subjected to selection in a medium containing 2 μCi/ml tritiated deoxyadenosine and 1 μg/ml deoxycoformycin, an inhibitor of adenosine deaminase. All resistant subclones were cross-resistant to tubercidin, 6-methylmercaptopurine riboside, and arabinosyladenine. One of the subclones, S49-12, was completely devoid of adenosine kinase and was partially deficient in deoxyadenosine kinase. This subclone, however, contained wild-type levels of deoxycytidine kinase. DEAE chromatography of the wild-type cell extracts revealed two deoxyadenosine phosphorylating activities, one of which coeluted with adenosine kinase and was the enzyme missing in S49-12. The other species phosphorylated both deoxyadenosine and deoxycytidine, of which deoxycytidine was the preferred substrate.

Original languageEnglish (US)
Pages (from-to)765-777
Number of pages13
JournalBiochemical Genetics
Volume25
Issue number11-12
DOIs
StatePublished - Dec 1987

Keywords

  • deoxyadenosine kinase
  • deoxycytidine kinase
  • nucleoside analogues
  • tritium suicide

ASJC Scopus subject areas

  • Ecology, Evolution, Behavior and Systematics
  • Biochemistry
  • Molecular Biology
  • Genetics

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