Sequence duplication and inverted repeats present in our data are also consistent with transposon insertion sites (Fig. 2).
RMSs were disrupted in the forms of partial gene deletion, internal sequence duplication, and insertion (IS) elements (fig. 5).
Domain shuffling/recombination, gene sequence duplication and divergence are three major mechanisms contributing to the evolution of organismal complexity [ 2].
For two of the annotated genes, FGSG_08274 and FGSG_12303, no specific oligonucleotide was identified, due to sequence duplication and repetitive sequence structure.
In general, the patterns of sequence conservation and positions of microsatellites suggest multiple mechanisms of sequence duplication and diversification within the Sp185/333 gene family.
SNPs have traditionally been thought to be the dominant source of sequence variation although other sequence variants, such as sequence duplication and deletion recognized microscopically [ 1], were described decades ago.
Recombination can also cause sequence duplications and deletions, resulting in rapid and sometimes substantial shifts in genome size.
Insertion at multiple positions, short target sequence duplications, and terminal inverted repeats (which typically constitute sites of transposase action) are characteristic of many classes of transposable elements [2], [4], [5].
Recombination events at conserved DNA sequences between paralogs, large sequence duplications, and transposable element insertions have contributed to the amplification and diversification of the rXA21 gene family [ 71].
This defense mechanism detects DNA sequence duplications and induces irreversible C G to T A mutations at a high rate in these sequences.
