@article {539626, title = {Self-inflicted wounds, template-directed gap repair and a recombination hotspot. Effects of the mariner transposase}, journal = {Genetics}, volume = {154}, number = {2}, year = {2000}, note = {

Lohe, A RTimmons, CBeerman, ILozovskaya, E RHartl, D LengGM-33741/GM/NIGMS NIH HHS/Research Support, Non-U.S. Gov{\textquoteright}tResearch Support, U.S. Gov{\textquoteright}t, P.H.S.2000/02/03 09:00Genetics. 2000 Feb;154(2):647-56.

}, month = {Feb}, pages = {647-56}, abstract = {

Aberrant repair products of mariner transposition occur at a frequency of approximately 1/500 per target element per generation. Among 100 such mutations in the nonautonomous element peach, most had aberrations in the 5{\textquoteright} end of peach (40 alleles), in the 3{\textquoteright} end of peach (11 alleles), or a deletion of peach with or without deletion of flanking genomic DNA (29 alleles). Most mariner mutations can be explained by exonuclease "nibble" and host-mediated repair of the double-stranded gap created by the transposase, in contrast to analogous mutations in the P element. In mariner, mutations in the 5{\textquoteright} inverted repeat are smaller and more frequent than those in the 3{\textquoteright} inverted repeat, but secondary mutations in target elements with a 5{\textquoteright} lesion usually had 3{\textquoteright} lesions resembling those normally found at the 5{\textquoteright} end. We suggest that the mariner transposase distinguishes between the 5{\textquoteright} and 3{\textquoteright} ends of the element, and that the 5{\textquoteright} end is relatively more protected after strand scission. We also find: (1) that homolog-dependent gap repair is a frequent accompaniment 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.

}, keywords = {*DNA Repair, *Recombination, Genetic, Animals, Animals, Genetically Modified, Base Sequence, DNA, Drosophila/genetics, Mutation, Templates, Genetic, Transposases/*genetics}, isbn = {0016-6731 (Print)0016-6731 (Linking)}, author = {Lohe, A. R. and Timmons, C. and Beerman, I. and Lozovskaya, E. R. and Hartl, D. L.} }