IS10 antisense control in vivo is affected by mutations throughout the region of complementarity between the interacting RNAs.
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.
Jain
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Department of Biochemistry and Molecular Biology, Harvard University, Cambridge, MA 02138.
D001483:Base Sequence; D003001:Cloning, Molecular; D004251:DNA Transposable Elements / Q000235:genetics*; D005786:Gene Expression Regulation / Q000235:genetics; D008969:Molecular Sequence Data; D009154:Mutation; D009713:Nucleotidyltransferases / Q000235:genetics*; D016372:RNA, Antisense / Q000235:genetics*; D012333:RNA, Messenger / Q000235:genetics; D019895:Transposases
D004251:DNA Transposable Elements; D016372:RNA, Antisense; D012333:RNA, Messenger; C095509:IS10 transposase; D009713:Nucleotidyltransferases; D019895:Transposases