Self-inflicted wounds, template-directed gap repair and a recombination hotspot: Effects of the mariner transposase

Aberrant repair products of mariner transposition occur at a frequency of s imilar to 1/500 per target element per generation. Among 100 such mutations in the nonautonomous element peach, most had aberrations in the 5' end of peach (40 alleles), in the 3' end of peach (11 alleles), or a deletion of p each with or without deletion of flanking genomic DNA (29 alleles). Most ma riner mutations can be explained by exonuclease "nibble" and host-mediated repair of the double-stranded gap created by the transposase, in contrast t o analogous mutations in the P element. In mariner, mutations in the 5' inv erted repeat are smaller and more frequent than those in the 3' inverted re peat, but secondary mutations in target elements with a 5' lesion usually h ad 3' lesions resembling those normally found at the 5' end. We suggest tha t the mariner transposase distinguishes between the 5' and 3' ends of the e lement, and that the 5' end is relatively more protected after strand sciss ion. We also find: (1) that homolog-dependent gap repair is a frequent acco mpaniment to mariner excision, estimated as 30% of all excision events; and (2) that mariner is a hotspot of recombination in Drosophila females, but only in the presence of functional transposase.