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Genetic control of radiation sensitivity and DNA repair in Neurospora

Conference ·
OSTI ID:4144516
Radiation sensitivity in the fungus Neurospora crassa is under the control of at least eight distinct loci and is also affected by cytoplasmic factors. Although radiation-sensitive mutants which affect inter- or intragenic meiotic recombination have not been isolated, mutants which are defective in the repair of pyrimidine dimers have been found. Evidence from both mutational and biochemical studies shows that Neurospora has an excision-repair system for pyrimidine dimers which is very similar to the one found in Escherichia coli. Wild-type strains excise dimers, but two mutants, uvs2 and upr1, are uv sensitive and excision defective. Like the E. coli excision-defective mutants, the Neurospora mutants show a greatly increased frequency of uv-induced mutation at low uv doses, and they do not affect recombination. However, they differ from the E. coli mutants in being significantly more sensitive to ionizing radiation than wild-type strains. A third mutant, uvs6, resembles the DNA polymerase-I- negative mutants of E. coli. It is sensitive to both uv and x-irradiation, has a wild-type pattern of uv-induced mutation, and increases spontaneous deletion frequencies. Its polymerases have not been examined. The high frequency of uv- induced mutation in excision-defective strains suggests that a ''mutation prone'' system of DNA repair exists in Neurospora. (auth)
Research Organization:
Washington State Univ., Pullman
NSA Number:
NSA-33-012303
OSTI ID:
4144516
Country of Publication:
United States
Language:
English