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pH induced damage and repair in E. coli.

J Musarrat1, M Ahmad

  • 1Department of Biochemistry, Faculty of Life Sciences, Aligarh Muslim University, India.

Mutation Research
|May 1, 1988
PubMed
Summary

Escherichia coli exposed to alkaline conditions lost colony-forming ability, with radiation-sensitive mutants showing decreased survival. Alkali-injured cells recovered partially, but mutants recA and lexA did not, indicating DNA repair pathway involvement.

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Area of Science:

  • Microbiology
  • Molecular Biology
  • Genetics

Background:

  • Alkaline environments can impact bacterial viability and DNA integrity.
  • Specific DNA repair mechanisms are crucial for bacterial survival under stress conditions.

Purpose of the Study:

  • To investigate the effects of alkaline stress on Escherichia coli survival and DNA repair.
  • To compare the response of wild-type E. coli and radiation-sensitive mutants (recA, polA, res, rer, lexA) to alkaline conditions.
  • To assess the recovery potential and mutagenesis induced by alkali treatment.

Main Methods:

  • Exposure of Escherichia coli (wild-type and mutants) to Tris/NaOH and Tris/Mg2+ buffers at pH 10.0 and 4.0.
  • Incubation of alkali-injured cells in phosphate buffer (pH 8.0) for recovery assessment.
  • Measurement of bacterial survival, UV sensitivity, and mutation frequency.
  • Analysis of alkali treatment effects on Salmonella typhimurium mutants TA102 and TA104.

Main Results:

  • Escherichia coli lost colony-forming ability in alkaline buffers (pH 10.0 and 4.0).
  • Radiation-sensitive mutants (recA, polA, res, rer, lexA) showed significantly reduced survival compared to wild-type.
  • Alkali-injured cells recovered in phosphate buffer, but recA and lexA mutants did not exhibit liquid holding recovery.
  • Alkali treatment enhanced UV sensitivity and mutagenesis in wild-type E. coli, while recA and lexA mutants showed no increase in mutation frequency.
  • Alkali treatment of Salmonella typhimurium mutants TA102 and TA104 resulted in a high number of revertants.

Conclusions:

  • Alkaline stress severely affects bacterial viability, particularly in DNA repair-deficient mutants.
  • Specific DNA repair pathways, like those involving recA and lexA, are essential for recovery from alkali-induced damage.
  • Alkali treatment induces mutagenesis, but this is dependent on functional DNA repair systems.
  • The study highlights the complex interplay between alkaline stress, DNA repair, and mutagenesis in bacteria.

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