DNA sequence analyses support the role of interrupted gap repair in the origin of internal deletions of the maize transposon, MuDR.

Previous research has demonstrated that the autonomous Cy transposon can activate the excision of Mu transposons. To determine the relationship between Cy and the more recently described autonomous Mu transposon, MuDR, a Cy transposon inserted at the mutable a1 allele, a1-m5216, was isolated and cloned. DNA sequence analyses established that this Cy insertion is identical to MuDR (Mu9, GenBank accession No.: m76978.gb-pl). Therefore, Cy will henceforth be termed MuDR:Cy. Defective derivatives of MuDR:Cy were isolated that had lost their capacity to activate their own excision or the excision of a Mu7 transposon. Most of these derivatives are nonautonomous transposons because they can excise, but only in the presence of unlinked MuDR:Cy transposons. Physical mapping and DNA sequence analyses have established that six of these defective derivatives carry internal deletions. It has been proposed previously that such deletions arise via interrupted gap repair. The DNA sequences of the break points associated with all four sequenced deletions are consistent with this model. The finding that three of the excision-defective derivatives carry deletions that disrupt the coding region of the mudrA (but not the mudrB) transcript supports the view that mudrA plays a role in the excision of Mu transposons.

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