Pietrzykowska I, Krych M, Shugar D
Mutat Res. 1983 Oct;111(2):119-33. doi: 10.1016/0027-5107(83)90057-x.
Lesions induced by 5-bromouracil (BU), after its incorporation into DNA, led to effective induction of prophage lambda and W reactivation (or BU reactivation). Prophage induction due to incorporated BU occurred only with the wild-type prophage, and not for the lambda c1857 mutant with a thermosensitive repressor. Antipain, a protease inhibitor, inhibited wild-type prophage induction 70-90%. This indicates that BU-induced lesions may induce the SOS repair system. The finding that such lesions provoke BU reactivation permits the inference that BU-induced mutagenesis also proceeds via involvement of the error-prone repair system, and not directly as a result of base-pairing errors. Genetic evidence suggests that induction of the SOS repair system as a result of incorporation of BU into DNA is linked to the subsequent appearance of uracil residues and apyrimidinic sites, resulting from dehalogenation of incorporated BU. Apyrimidinic sites appear to be more effective than uracil residues in induction of the SOS system.
5-溴尿嘧啶（BU）掺入DNA后所诱导的损伤，导致了原噬菌体λ的有效诱导和W复活（或BU复活）。由于掺入的BU而引起的原噬菌体诱导仅发生在野生型原噬菌体中，而对于带有热敏阻遏物的λc1857突变体则不会发生。抗蛋白酶（一种蛋白酶抑制剂）抑制野生型原噬菌体诱导达70 - 90%。这表明BU诱导的损伤可能诱导SOS修复系统。此类损伤引发BU复活这一发现允许推断，BU诱导的诱变也通过易错修复系统的参与而进行，并非直接由于碱基配对错误。遗传学证据表明，由于BU掺入DNA而导致的SOS修复系统的诱导与随后尿嘧啶残基和脱嘧啶位点的出现有关，这些是由掺入的BU脱卤作用产生的。脱嘧啶位点在诱导SOS系统方面似乎比尿嘧啶残基更有效。
