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Defective excision repair in a mutant of Micrococcus radiodurans hypermutable by some monofunctional alkylating

P R Tempest, B E Moseley

    Molecular & General Genetics : MGG
    |January 1, 1980
    PubMed

    Insights

    A Micrococcus radiodurans mutant (strain 302) shows differential sensitivity to DNA damaging agents. This mutant exhibits hypermutability due to unrepaired base modifications, while lethality stems from unrepaired base-pair disruptions.

    Area of Science:

    • Microbiology
    • Genetics
    • Molecular Biology

    Background:

    • Micrococcus radiodurans is known for its exceptional radiation resistance.
    • Understanding DNA repair mechanisms is crucial for comprehending microbial resistance and mutagenesis.

    Purpose of the Study:

    • To investigate the differential lethal and mutagenic effects of various DNA damaging agents on a mitomycin C (MTC)-sensitive mutant (strain 302) of Micrococcus radiodurans.
    • To elucidate the underlying mechanisms of hypermutability and lethality in this mutant.

    Main Methods:

    • Comparative analysis of sensitivity to methyl methanesulphonate (MMS), ethyl methanesulphonate (EMS), N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), and other agents in strain 302 versus wild-type.
    • Alkaline sucrose gradient centrifugation to study DNA incision following exposure to 7-bromomethylbenz[alpha]anthracene (BrMBA) and N-acetoxy-N-2-acetylaminofluorene (AAAF).

    Main Results:

    • Strain 302 displays extreme sensitivity to MTC and decarbamoyl MTC (DCMTC), slight sensitivity to EMS and MNNG, and resistance to MMS.
    • The mutant is highly mutable by MMS, EMS, and MNNG, unlike the wild type.
    • Alkaline sucrose gradients suggest impaired DNA incision for BrMBA adducts and possibly reduced incision for AAAF-damaged DNA in strain 302.

    Conclusions:

    • The hypermutability of strain 302 is hypothesized to result from the accumulation of unrepaired base modifications with altered base-pairing capabilities.
    • Lethality in this mutant is proposed to arise from the persistence of unrepaired base modifications that disrupt hydrogen bonding in base pairs.

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