Differential repair of UV damage in a developmentally regulated gene of Dictyostelium discoideum
| Autor: | Stanley K. Mauldin, Reginald A. Deering, Thomas M. Freeland |
|---|---|
| Rok vydání: | 1994 |
| Předmět: |
Xeroderma pigmentosum
DNA Repair Ultraviolet Rays DNA repair DNA damage Mutant Pyrimidine dimer Toxicology Dictyostelium discoideum chemistry.chemical_compound Gene Expression Regulation Fungal Cyclic AMP Genetics medicine Animals Dictyostelium DNA Fungal Molecular Biology Gene biology biology.organism_classification medicine.disease Molecular biology Cysteine Endopeptidases chemistry Cyclobutanes DNA DNA Damage |
| Zdroj: | Mutation Research/DNA Repair. 314:187-198 |
| ISSN: | 0921-8777 |
| Popis: | The repair of cyclobutane pyrimidine dimers was measured under non-replicating conditions in a 2054-bp fragment of a cAMP-inducible cysteine proteinase (CP2) gene in D. discoideum. Overall genomic repair was unaffected by cAMP. The removal of dimers from CP2 in the wild-type NP2 cells as quantified using T4 endonuclease V was independent of transcription and was the same as in the overall genome. In a UV-sensitive radC mutant in which the rate of overall dimer removal was previously shown to be reduced, the initial rate of dimer removal in the uninduced CP2 gene (-cAMP) was 3-fold lower compared to the induced gene (+cAMP), in which repair was identical to that for the induced and uninduced states of NP2. D. discoideum may have two pathways for repairing dimers. One, effective in the wild-type strain but of reduced efficiency in radC repairs dimers equally well independent of transcription and at about the same rate as in the overall genome. A second pathway, retained in radC, repairs dimers more slowly in the overall genome and in the uninduced CP2 gene while undergoing the wild-type rate of repair in the transcriptionally active gene. Hence radC has reduced ability to repair transcriptionally inactive DNA, a defect similar to that of xeroderma pigmentosum group C. |
| Databáze: | OpenAIRE |
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