Abstract
The excision repair capacity of the third chromosomal mus mutations of Drosophila has been re-evaluated. A partial deficiency in the excision repair of pyrimidine dimers originally observed in the mus304 mutants is now attributed to the presence of a secondary phr mutatiuon in that stock. Since the mus306 and mus308 stocks also carry secondary phr mutations, their partial deficiency in repair of pyrimidine dimers may also be the result of that secondary mutation. Accordingly, the Drosophila mutations that are now definitively associated with defects in the incision step of pyrimidine dimers removal are mei-9, mus 201 and phr. The genes mus302 and mus310 appear to play a role in later stages of excision repair.
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