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Exact(5)
In 12 of the 20 families, new family members are found on the same scaffold in close proximity suggesting unequal crossing over or proximate segmental duplication as the mechanisms for duplicate formation.
A challenge in evolutionary biology, then, is to identify the relative importance of different mechanisms for duplicate gene retention, and also to understand what genetic factors prior to duplication portend a high probability of both paralogs persisting as functional loci after duplication.
Thus, in addition to supporting mechanisms based on dosage balance and pleiotropy, our results are also consistent with mechanisms for duplicate gene retention that involve regulatory subfunctionalization.
Additionally, some of these mechanisms for duplicate gene retention are not mutually exclusive and could operate concurrently or sequentially [ 28, 32] and this could also be associated with temporal changes in functional constraints.
The model has been validated on simulated data and subsequent analysis with the model on genomic data from human and mouse shows that conclusions about the underlying mechanisms for duplicate gene retention can be sensitive to consideration of population genetic processes.
Similar(55)
Moreover, known mechanisms for duplicating and inserting copies of a complex DNA signal at multiple locations generally disrupt coding capacity.
The involvement of the duplicated TFIIAγ genes in adversity response could also be explained by the buffering hypothesis [ 27], which suggests that selection for a buffering effect was a mechanism for duplicate gene preservation after whole genome duplication.
However, if neofunctionalizing mutations are rare or not very advantageous, or if population size is small, pre-duplication neofunctionalization is unlikely to be a common mechanism for duplicate gene persistence [ 18, 19], although clearly it has occurred [ 20].
Subcellular relocalization has previously been described as a mechanism for duplicate gene retention [53] [55] and as a factor contributing to asymmetric sequence divergence [56].
These results suggest that subcellular relocalization is unlikely to have been a major mechanism for duplicate gene retention and functional divergence at the genomic scale.
Mechanistic models have previously been introduced that allow for probabilistic inference of the evolutionary mechanism for duplicate gene retention based upon the average rate of loss over time of the duplicate.
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