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It appears that the forces causing tandem repeats such as mutation, replication slippage etc., occurred more frequently in non-coding regions than the genic regions [ 22, 45, 47].
First, the above-mentioned double OL-like structures initiated DNA synthesis twice during mitochondrial replication, causing tandem duplication of the genes located between the CR and the WANCY region (1 13) in the ancestral mitogenome.
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It is also known that recombination processes may cause tandem duplications [42] locally and, in our view, distantly on different strands [43], [44].
Previous studies in C. elegans have shown that transposable elements can cause tandem duplications [ 33].
These arrays suggest that repeated gene conversion can cause tandem duplicates to evolve in concert, in the presence of neutral divergence (or even positive selection).
The chimeric WldS gene resulted from a spontaneous mutation in the C57BL/6 line of mice, causing a tandem triplication in the distal region of chromosome 4 [20].
Lower NCE resulted in poor fragmentation of the selected precursor ion, so fewer product ions were generated, causing poor tandem mass spectra matching.
It occurs on every scale within the genome: mistakes during DNA synthesis cause tandem duplication of individual genes, and segmental duplication often results from the transposition of mobile elements; for instance, the transposition of an Alu element caused the duplication of the human BRCA1 region [ 13].
Finally, we found polar residues to be slightly enriched in tandem donor and strongly enriched in tandem acceptor protein contexts, which is further evidence that protein variations caused by tandem acceptors are preferentially located on the surface of folded domains.
To avoid biases caused by tandem duplications, we removed all such pairs from our analyses.
In most cases the MP transcript of the second step is also ML but there are exceptions caused by tandem repeats or if the mitochondrial phylogeny suggests otherwise as discussed in example 2 below.
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