{'fraction_non_alphanumeric': 0.025182778229082048, 'fraction_numerical': 0.017871649065800164, 'mean_word_length': 5.190954773869347, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Genesis and natural history of IS-mediated transposons.

The natural genesis of IS1-mediated transposons containing the genetic determinant cat for chloramphenicol resistance is documented. First, the small plasmid pBR325 containing the cat gene served as a target in IS1-mediated transpositional cointegration with the genome of bacteriophage P1, which was the source of the IS1. From the resulting pBR325:P1 plasmids, pBR325::IS1 segregants were isolated. Upon growth of a phage lambda derivative in the presence of this plasmid, rare plaque-forming lambda Cmr specialized transducing phages were formed. In each of six independent lambda Cmr isolates studied, the cat gene was carried between flanking IS1 elements. In one case, these IS1 elements were in the same orientation; in the other five cases, they were in opposite orientation. All of these IS1-cat-IS1 structures transposed as units to the genome of phage P1-15, pointing to stable maintenance of the transposon. However, appropriate selection allowed us to follow the decay of these transposons. Models to explain the genesis of transposons with directly and inversely repeated IS elements are discussed, as well as the evolutionary implications of these mechanisms.