A Specific Class of IS10 Transposase Mutants Are Blocked for Target Site Interactions and Promote Formation of an Excised Transposon Fragment

Cell. 1989 Oct 20;59(2):385-94. doi: 10.1016/0092-8674(89)90299-7.


We report the identification and characterization of a class of IS10 transposase mutants that carry out only some of the steps required for transposition. These mutants were identified among transposition-defective mutants as a specific subclass that retains the wild-type ability to induce SOS functions in the presence of transposon ends. Mutants of this class successfully promote excision of the element from its donor site, but do not promote transfer of the transposon sequences to a target site. SOS induction presumably results from the degradation of the donor site. Uniquely among transposition-defective mutants, SOS+ Tnsp- mutants promote the formation of a new product, the excised transposon fragment (ETF), which consists of the transposon excised from the original donor molecule by double-strand breaks at the transposon ends. SOS+ Tnsp- mutants identified thus far define two patches of amino acids that might correspond to regions of different function. A single additional mutation maps within a region that is highly conserved among IS element transposases. The existence of SOS+ Tnsp- mutants and the structure of the ETF provide strong support for the previously proposed nonreplicative model of Tn10/IS10 transposition.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Alleles
  • DNA Transposable Elements*
  • Escherichia coli / enzymology
  • Escherichia coli / genetics*
  • Genes, Bacterial
  • Mutation*
  • Nucleotidyltransferases / genetics*
  • Phenotype
  • Plasmids
  • Restriction Mapping
  • SOS Response, Genetics
  • Transposases


  • DNA Transposable Elements
  • Nucleotidyltransferases
  • Transposases