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KMID : 0379119880160030000
Korean Journal of Mycology
1988 Volume.16 No. 3 p.0 ~ p.0
Uv mutagenesis in Aspergillus nidulans
Han Dong-Min
Abstract
The homothallic ascomycetes, Aspergillus nidulans, has a number of experimentally advantageous features. It grows rapidly on simple synthetic media and produces a large number of asexual spores which are arrested at G1 stage. It also reproduces sexually and parasexually, which provides the useful tools for genetic analyses.
Aspergillus nidulans strains were easily mutagenized by the various mutagens including Ultraviolet radiation and some alkylating agents. The induction of mutation by these mutagens were not passive process and several genes were required for the process. This was confirmed by the isolation of the mutants non-mutable with UV or some alkylating agents. A mutant strain, UVS H1, was defective in the UV mutagenesis only, indicating that an error-prone DNA repair pathway which specifically responsed to the damages induced by UV or UV mimetic mutagens might exist in Aspergillus nidulans. It did not show any defects in growth, development or recombinational behaviour. An allelic mutant did not have any different phenotype. The results suggested that uvsH gene be directly involved in the UV mutagenesis.
Asexual spore cells in G1 stage were sensitive to both cell lethality and mutation induction with UV irradiation. The sensitivity reached to the maximum just before the S stage. The rate of mutation induction was decreased when the cells committed the DNA replication to a certain extent. The UVS H mutants, which was blocked in UV mutagenesis in all the stages of the cell division cycle, showed significant sensitivity only in the pre-replicative phase. The mutations induced by UV radiation were not fully photoreversed, indicating the DNA lesion other than pyrimidine dimer also acted as premutagenic lesion. The mutations that were photoreversible were fixed during DNA replication. These results suggested that the induction of mutation be dependent on the number of unrepaired lesions that reach the replicating fork or of those that occur at that time, and that the error-prone DNA repair play an important role in the increasing the potential for survival by achieving the fidelity of DNA replication in compensation for the mutation.
The experimental results of mutation kinetics, split-dose irradiation and the effect of cycloheximide on the UV mutagenesis suggested that the mutagenic processes were rather constitutive than inducible.
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