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The dataset of human and mouse transposed element exonization was obtained from the TranspoGene database [39].
In mouse, for all transposed element families, the density of SNPs in exonized TEs was significantly higher than the overall density in all TEs (Mann-Whitney test, p = 0.004, two-tailed).
Exonization is an event which an intronic transposed element (TE) provides splice sites and leads to alternatively spliced cassette exons.
This would agree with phylogenetic studies using transposed element insertions showing that during periods of rapid speciation of placental mammals such markers can be polymorphic (unfixed) and phylogenetically unreliable due to incomplete lineage sorting (Churakov et al., 2009).
Sela N, Mersch B, Gal-Mark N, Lev-Maor G, Hotz-Wagenblatt A, Ast G. Comparative analysis of transposed element insertion within human and mouse genomes reveals Alu's unique role in shaping the human transcriptome.
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In the symmetric matrix, an asterisk "∗" is used to denote the transposed elements.
Actively and/or recently transposed elements belonging to the same family should be nearly identical in sequence, whereas inactive transposons may be diverged to such an extent that they will be unidentifiable.
SNP density analysis revealed differences between Alu and other transposed elements.
Insertion of transposed elements within mammalian genes is thought to be an important contributor to mammalian evolution and speciation.
Alu elements were inserted into the human genome after the insertion of other families, such as MIRs, DNA transposed elements, and LTRs [64].
The draft sequences of the human and mouse genomes confirmed that transposed elements (TEs) have played a major role in shaping mammalian genomes [1], [2].
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