Davis M A, Simons R W, Kleckner N
Cell. 1985 Nov;43(1):379-87. doi: 10.1016/0092-8674(85)90043-1.
Tn10 rarely transposes, primarily because its IS10-encoded transposase protein is synthesized infrequently. Since the 5' end of the transposase gene is immediately adjacent to flanking host sequences, insertion of Tn10 into an actively transcribed operon could conceivably result in dramatically increased transposition. We show here that Tn10 is protected from such fortuitous activation; high levels of transcription from an upstream promoter actually decrease its rate of transposition. Protection operates at two levels. First, externally-initiated transcripts yield only a small amount of additional transposase protein, primarily because of inhibition at a posttranscriptional level. We suggest that the transposase gene start codon is sequestered in an mRNA secondary structure not present in transcripts initiated at the normal promoter. Second, transcription per se across an IS10 terminus inhibits its activity, thus negating any small transposase increase. These observations provide additional evidence that Tn10 has evolved specific mechanisms for keeping its transposition activity low.
Tn10很少发生转座，主要是因为其由IS10编码的转座酶蛋白合成频率很低。由于转座酶基因的5'端紧邻侧翼宿主序列，因此将Tn10插入到一个活跃转录的操纵子中可能会显著增加转座频率。我们在此表明，Tn10能免受这种偶然激活的影响；来自上游启动子的高水平转录实际上会降低其转座速率。这种保护作用在两个层面发挥作用。首先，外部启动的转录本仅产生少量额外的转座酶蛋白，主要是因为在转录后水平受到抑制。我们认为转座酶基因起始密码子被隔离在正常启动子起始的转录本中不存在的mRNA二级结构中。其次，跨IS10末端本身的转录会抑制其活性，从而抵消转座酶的任何少量增加。这些观察结果提供了额外的证据，表明Tn10已经进化出特定机制来保持其低转座活性。
