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[W-mutagenesis in the bisulfite-treated lambda phage].

L V Konevega, V L Kalinin

|July 1, 1985

Summary

Bisulfite inactivation of phage lambda cI857 is less effective in wild-type bacteria (ung+) due to SOS repair mechanisms. This DNA repair pathway influences the frequency of mutations induced by bisulfite treatment.

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Area of Science:

Molecular Biology
Genetics
Microbiology

Background:

Bisulfite is a chemical mutagen that deaminates cytosine bases in DNA.
The uracil-DNA glycosylase (UNG) enzyme excises uracil from DNA, a product of cytosine deamination.
SOS repair is a DNA damage response system in bacteria.

Purpose of the Study:

To investigate the role of uracil-DNA glycosylase (UNG) and SOS repair in the inactivation and mutagenesis of phage lambda cI857 by bisulfite.
To understand the mechanisms underlying bisulfite-induced mutations in bacteriophage DNA within different bacterial host strains.

Main Methods:

Inactivation assays of phage lambda cI857 treated with bisulfite on lawns of wild-type (ung+) and ung-1 mutant bacteria.
UV irradiation of host cells to induce the SOS repair system prior to bisulfite treatment.
Quantification of phage survival and mutation frequencies.

Main Results:

Phage lambda cI857 showed higher survival and lower mutation frequency when inactivated by bisulfite on wild-type (ung+) lawns compared to ung-1 mutant lawns.
UV-induced SOS repair in wild-type (ung+) hosts significantly increased the frequency of bisulfite-induced mutations, an effect not observed in ung-1 mutants.
The dose modification factor for bisulfite inactivation was approximately 1.2 in favor of the ung+ strain.

Conclusions:

The uracil-DNA glycosylase (UNG) proficient host (ung+) exhibits enhanced protection against bisulfite-induced phage inactivation.
SOS repair in ung+ cells promotes mutagenesis by bisulfite, likely through the repair of apyrimidinic sites generated by uracil excision.
These findings suggest a complex interplay between DNA repair pathways and chemical mutagenesis in bacteriophages.

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