Jain C
Department of Biochemistry and Molecular Biology, Harvard University, Cambridge, MA 02138.
J Mol Biol. 1995 Mar 10;246(5):585-94. doi: 10.1016/s0022-2836(05)80108-1.
Translation of the IS10 transposase mRNA (RNA-IN) is inhibited by antisense pairing with a small IS10 encoded transcript called RNA-OUT. To further characterize IS10 antisense control, an extensive set of mutations in the region of complementarity between RNA-OUT, and its target RNA-IN have been isolated. These mutations have been characterized for their effects on antisense inhibition of transposase gene translation in vivo. Mutations that confer the strongest defects on translational inhibition are found in the region corresponding to the 5' end of RNA-IN. However, mutations throughout the complementary region affect antisense control regardless of whether mutations are present in RNA-IN alone or as complementary mutations in both RNAs. An analysis of the data presented here suggests that in vivo pairing rates for the wild-type antisense species are very close to being optimal. Some of the motifs found in antisense molecules that may be associated with efficient pairing rates are discussed.
IS10转座酶mRNA(RNA-IN)的翻译受到与一种名为RNA-OUT的小的IS10编码转录本的反义配对的抑制。为了进一步表征IS10反义调控,已分离出RNA-OUT与其靶RNA-IN之间互补区域的大量突变。这些突变已针对其对体内转座酶基因翻译的反义抑制作用进行了表征。在与RNA-IN的5'端相对应的区域中发现了对翻译抑制具有最强缺陷的突变。然而,整个互补区域的突变都会影响反义调控,无论突变是仅存在于RNA-IN中还是作为两个RNA中的互补突变。此处呈现的数据分析表明,野生型反义物种的体内配对率非常接近最佳值。讨论了在反义分子中发现的一些可能与高效配对率相关的基序。