We have studied some of the products of abnormal excision of prophage λ . Abnormal excision occurs when an excision enzyme is lacking (as in the case of int or xis mutants) or when a prophage attachment site is altered (as in the case of prophage λb 2). As described earlier (Gottesman and Yarmolinsky, 1968), induction of a lysogen of λb 2 yields primarily a dense phage which transduces the bacterial genes bio and uvrB . Production of this phage requires either red or rec function. The transducing phage in turn yields, at a low rate, nontransducing phage with the properties of the original phage parent λb 2; this reversion is dependent on a functional int gene. On the basis of this instability it was proposed that the transducing phage denoted λb 2 att 2 has the structure depicted in Fig. 1, and arises because normal excision is blocked by the defect in the right-hand attachment site of a λb 2 prophage (Zichichi and Kellen-berger, 1963; Campbell, 1965; Fischer-Fantuzzi, 1967; Parkinson, 1970). As can be seen in Fig. 1, a transducing phage denoted λatt 2 , which arises by general recombination at homology regions outside the prophage attachment sites, would include the two hybrid attachment sites which bracket the prophage genome. The reversion of this transducing phage to the original nontransducing phage would be analogous to prophage excision, i.e., the result of recombination of these two attachment sites. The slow rate of reversion of λb 2 att 2 to λb 2 would appear to be a consequence of the b 2 attachment site defect. To obtain...
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Shulman et al. (1971) studied this question.