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Reversion in thymidine kinase deficient variants of mouse lymphoma P388

S M Ruddy1, I Hickey

  • 1Department of Biology, The Queen's University of Belfast, Northern Ireland.

Mutation Research
|November 1, 1989
PubMed

Insights

Spontaneous reversion of thymidine kinase deficiency in mouse lymphoma cells was not observed. However, low-frequency reversion was induced by 5-azacytidine and EMS, suggesting stable gene inactivation.

Area of Science:

  • Molecular Biology
  • Genetics
  • Cancer Research

Background:

  • Mouse lymphoma P388 cells were used to study gene reversion.
  • Thymidine kinase deficiency was observed in 5 independently isolated clones.

Purpose of the Study:

  • To investigate the reversion frequency of thymidine kinase-deficient mouse lymphoma P388 clones.
  • To determine the effect of 5-azacytidine and EMS on reversion.
  • To analyze thymidine kinase activity in revertant cells.

Main Methods:

  • Isolation of 5 thymidine kinase-deficient clones from mouse lymphoma P388.
  • Treatment of clones with 5-azacytidine (a hypomethylating agent) and EMS (a mutagen).
  • Measurement of thymidine kinase activity in revertant cells.

Main Results:

  • No spontaneous revertants were detected in any of the 5 clones.
  • 5-azacytidine induced low-frequency reversion (<10^-6) in 4 clones, independent of dose.
  • EMS induced reversion in 3 clones with variable response.
  • 16 revertants showed thymidine kinase activity, with half exhibiting levels higher than the original P388 cell line.

Conclusions:

  • Spontaneous reversion is rare in these thymidine kinase-deficient clones.
  • Chemical agents can induce reversion, but at low frequencies.
  • High-frequency loss of thymidine kinase may indicate stable gene inactivation rather than DNA sequence alteration.

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