Three promoters near the termini of IS10: pIN, pOUT, and pIII

Abstract

We have identified three IS10-encoded promoters, pIN, the promoter for IS10's transposase gene, is intrinsically weak, contributing to the low frequency of IS10 transposition in vivo. Its transcripts begin near the "outside" end of IS10 and extend inward across the element. pOUT, a strong promoter just internal to and opposing pIN, directs transcription outward. Its transcripts are proposed to inhibit translation of the transposase gene in trans (accompanying paper). pOUT may also inhibit transcription from pIN in cis. pIII, a weak promoter near the "inside" end of IS10, is of unknown genetic importance. Many transposable elements activate, by adjacent insertion, silent genes lacking normal promoters. Such IS10-promoted turn-on is mediated by pOUT and results from continuation of pOUT-initiated transcripts past the IS10 terminus, into adjoining chromosomal material. Wild-type and mutant IS10 promoters have been analyzed in vitro. pIN is weaker than pOUT because of inefficient isomerization from closed to open complexes. Despite their proximity, pIN and pOUT do not interact before or during open complex formation.