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Photolysis of tritium‐labelled thymine‐derived photoproducts by 254‐nm ultraviolet radiation (u.v.) in conidia of Streptomyces griseus was measured by chromatography of cell hydrolysates. The relative photolysis cross‐sections of uracilthymine dimer (UT○) at various wavelengths are the same as those of thymine‐thymine dimer (TT○), and their ratios at 313, 365, 405 and 436 nm are 2:1:2:3. Except at 436 nm, these relative values agree very well with cross‐sections previously reported for photoreactivation of u.v. killing in this organism, leading to the conclusion that photoreactivation in the wild type is due to repair of cyclobutane‐type pyrimidine dimers. In a mutant showing restricted photoreactivation ( S. griseus PHR‐1), post‐u.v. treatments at the above wavelengths did not affect UT○ and TT○ in the conidia, supporting the earlier suggestion that this organism does not contain active PR enzyme. Another u.v. photoproduct, the precursor of a pyrimidine adduct (PO‐T) that appears in cell hydrolysates, was removed from both wild‐type and mutant cells very efficiently at 313 nm. This is presumably a direct photochemical reaction. In addition, in wild‐type cells, the precursor of PO‐T appeared to be inefficiently removed photoenzymatically at all wavelengths. Removal of the precursor of PO‐T appears to be biologically significant, however, only in the mutant.
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Ikenaga et al. (1971) studied this question.
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