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In contrast to other PTPs which are relatively fixed, these PTPs have undergone a recent evolutionary burst which resulted in new PTP alleles or copies, and in several cases the evolution of these PTPs follow models of duplication that involve positive selection of one of the duplicated gene copies [ 41].
Thus, most current approaches for duplication analysis rely on heuristics, approximation algorithms, or restricted models of duplication [ 3- 7].
Different models of duplication retention imply different predictions about substitution rates in the coding portion of paralogs and about asymmetry of these rates.
This phenomenon is likely to make detection of neo- and subfunctionalization signatures difficult, as these models of duplication retention also predict asymmetries in substitution rates and expression profiles.
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Therefore, the tubulin duplicates were also not derived by the classical model of duplication and divergence (Ohno 1970), which states that a duplicated gene will only be retained if it developed a totally new function (neofunctionalization).
This argues against the classical model of duplication and divergence [ 60], as without positive selection, in most cases a duplicate gene would be lost before finding novel function.
Such model of duplication may occur in two ways.
However, this improvement is confined to a constrained model of duplication histories.
One hypothesis proposed to explain these conserved mosaic patterns is a two-step model of duplication [ 14].
The second consists of the trees reconstructed by the PhylDog method (Boussau et al., 2012), with an explicit model of duplication and losses of trees.
A null model of duplication was implemented using GenPhyloData, a tool that simulates random "guest" trees along a known host phylogeny [ 27].
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