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Various models of genomic duplications, e.g. the duplicative transposition or the endoduplication, have been documented.
There are three main molecular mechanisms leading to new duplicates [ 2, 3]: 1) unequal crossing-over during homologous recombination, 2) duplicative transposition at the DNA level and retroposition mediated by mRNA, and 3) polyploidization.
The duplicative transposition of a genomic block of material (1 100 kb) leads to segmental duplications within a chromosome/genome [ 10], which are also known as low copy repeat sequences, that mediate recurrent chromosomal structural rearrangements [ 4].
In three of the 28 cases studied, the active BES was replaced by duplicative transposition of the entire new BES.
One hypothesis for this dual relationship is that these miRNAs could protect against too high rates of duplicative transposition, which would destroy the genome.
One hypothesis for this dual relationship is that these miRNAs could protect against too high rates of duplicative transposition, which would destroy the genome [34].
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In contrast to duplicative transpositions, endoduplications originate from tandem duplication events of local chromosomal regions mediated by unequal crossover.
Although inversions are thought to be the predominant mode of gene rearrangement in chloroplast genomes (Palmer 1991; Boudreau and Turmel 1995, 1996), we cannot exclude the possibility that other evolutionary mechanisms, such as transpositions or duplicative transpositions are responsible for some of the observed changes in gene order between the Stigeoclonium and Schizomeris cpDNAs.
Formation of adjacent deletions resulting from duplicative intramolecular transposition could also result in a single copy of the direct repeat located on each of the reciprocal deletion products [ 16].
Another surprising finding was the high frequency of segmental reversals and trans-chromosomal events (translocations and duplicative segmental transpositions) (Fig. 6).
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