The repair of UV-irradiated DNA of plasmid pBB29 was studied in an incision-defective rad3-2 strain of Saccharomyces cerevisiae and in a uvrA6 strain of Escherichia coli by the measurement of cell transformation. Plasmid pBB29 used in these experiments contained as markers the DNA of nuclear yeast g
The role of pyrimidine dimers in postreplication repair in Neurospora
β Scribed by Calza, Roger E. ;Schroeder, Alice L.
- Publisher
- Springer
- Year
- 1982
- Tongue
- English
- Weight
- 834 KB
- Volume
- 186
- Category
- Article
- ISSN
- 0026-8925
No coin nor oath required. For personal study only.
β¦ Synopsis
Using the Micrococcus luteus dimer specific endonuclease assay of Wilkins (1973), and photoreactivation we have examined the induction and fate of ultraviolet induced pyrimidine dimers in the excision defective strain, uvs-2, of Neurospora crassa.
Dimer induction was fluence dependent from 0 to 800 ergs/ mm 2 UV. An interdimer distance of 19.6 x 106 DNA molecular weight was found after a fluence of 220 ergs/mm 2. We confirm the earlier report that this mutant is completely excision defective (Worthy and Epler 1972). Photoreactivation (PR), which greatly enhanced survival (by 10 fold after 440 ergs/mm 2 UV), reduced significantly (4044%) the number of UV-endonuclease sensitive sites found in irradiated DNA. This treatment also alleviated immediately some of the temporary blocks to high molecular weight DNA synthesis (elongation or ligation) seen in irradiated cells.
We have also attempted to elucidate the mechanism of cellular postreplication repair used to overcome the UV inhibition to DNA synthesis. It was determined that during postreplication repair, Neurospora does not use recombination to bypass dimers and that single stranded DNA gaps opposite dimers do not appear to be present during the time when DNA being synthesized is made only in short pieces.
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