Simons R W, Kleckner N
Cell. 1983 Sep;34(2):683-91. doi: 10.1016/0092-8674(83)90401-4.
We present genetic evidence that insertion sequence IS10, the active element in transposon Tn10, can negatively control expression of its own transposase protein at the translational level. This control process is manifested in trans in a phenomenon called "multicopy inhibition": the presence of a multicopy plasmid containing IS10 inhibits transposition of a single copy chromosomal Tn10 element by reducing its ability to express transposition functions. Fusion analysis suggests that expression is reduced at the translational and not the transcriptional level. Only the outer 180 bp of IS10-Right are required on the plasmid for full inhibition. Plasmid-encoded transposase protein is not involved. The genetic structure of the essential plasmid region and the effects of point and deletion mutations on multicopy inhibition lead us to propose that inhibition of transposase translation occurs by direct pairing between the transposase messenger RNA and a small, complementary, regulatory RNA specified by the IS10-encoded pOUT promoter.
我们提供了遗传学证据，表明转座子Tn10中的活性元件插入序列IS10可在翻译水平上对其自身转座酶蛋白的表达进行负调控。这一调控过程以一种称为“多拷贝抑制”的现象在反式作用中体现：含有IS10的多拷贝质粒的存在会通过降低其表达转座功能的能力来抑制单拷贝染色体Tn10元件的转座。融合分析表明，表达在翻译水平而非转录水平降低。质粒上仅需IS10-Right的外侧180 bp即可实现完全抑制。这一过程不涉及质粒编码的转座酶蛋白。必需质粒区域中的遗传结构以及点突变和缺失突变对多拷贝抑制的影响，使我们提出转座酶翻译的抑制是通过转座酶信使RNA与由IS10编码的pOUT启动子指定的小的互补调节RNA之间的直接配对而发生的。
