IS10 antisense control in vivo is affected by mutations throughout the region of complementarity between the interacting RNAs

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12 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)585-594
Number of pages10
JournalJournal of Molecular Biology
Volume246
Issue number5
DOIs
StatePublished - Jan 1 1995
Externally publishedYes

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RNA
Mutation
Transposases
Messenger RNA
Genes

Keywords

  • antisense RNA
  • complementarity
  • IS10
  • mutational analysis
  • translational repression

ASJC Scopus subject areas

  • Molecular Biology
  • Virology

Cite this

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title = "IS10 antisense control in vivo is affected by mutations throughout the region of complementarity between the interacting RNAs",
abstract = "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.",
keywords = "antisense RNA, complementarity, IS10, mutational analysis, translational repression",
author = "Chaitanya Jain",
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AB - 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.

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KW - translational repression

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