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On the ability of Salmonella typhimurium cells to form deoxycytidine nucleotides

Molecular & General Genetics : MGG
|June 8, 1977
PubMed

Insights

Salmonella typhimurium mutants resistant to 5-fluorodeoxycytidine (FdCyd) lack deoxycytidine kinase. This study confirms that FdCyd resistance in S. typhimurium selects for dual defects in cytidine deaminase and deoxycytidine kinase.

Area of Science:

  • Microbiology
  • Molecular Biology
  • Biochemistry

Background:

  • Salmonella typhimurium mutants resistant to 5-fluorodeoxycytidine (FdCyd) are known to lack deoxycytidine kinase activity.
  • Previous screening methods for FdCyd resistance may inadvertently select for multiple genetic defects.

Purpose of the Study:

  • To investigate whether screening for FdCyd resistance in S. typhimurium selects for double mutants defective in both cytidine deaminase and deoxycytidine kinase.
  • To confirm the absence of deoxycytidine kinase activity in a broader range of S. typhimurium strains.

Main Methods:

  • Construction of a cdd mutant of S. typhimurium through P1-mediated gene transfer.
  • Assay of deoxycytidine kinase activity in the constructed transductants.
  • Discussion of 5-fluorodeoxycytidine toxicity and the role of nucleoside phosphorylase.

Main Results:

  • Transductants derived from the cdd mutant consistently exhibited no detectable deoxycytidine kinase activity.
  • The absence of deoxycytidine kinase activity was demonstrated to be a characteristic of S. typhimurium strains selected for FdCyd resistance, not limited to a single mutant.

Conclusions:

  • The screening method for 5-fluorodeoxycytidine resistance in S. typhimurium effectively selects for double mutants lacking both cytidine deaminase and deoxycytidine kinase.
  • The findings highlight the importance of understanding enzymatic pathways for drug resistance mechanisms in bacteria.

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