Abstract:
Tn9, like other transposable elements, promotes formation of deletions. This activity has been monitored using a plasmid (pAA3B101) on which deletions can be selected positively as galactose-resistant colonies. Measurements of deletion formation by a series of internal deletions of Tn9, generated by restriction endonucleases, show that the two IS1 elements of Tn9 are functionally non-equivalent. IS1-L is active while IS1-R is inactive. The inactive IS1-R element can, however, be reactivated by a deletion which specifically removes the cat promoter. This result indicates that the inactivity of IS1-R is not due to an altered sequence (Galas & Chandler, 1982), but due to inhibition by transcription from the cat promoter (Machida et al., 1983) which acts in a direction opposite to IS1-R transcription. The occurrence of non-equivalent IS in all transposons analysed suggests that this may be an important feature of organization required for the stability of these composite elements.
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