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This suggests that although duplicate genes within the same complex may be frequently redundant, the majority of redundancy within complexes cannot be explained by duplication.
For instance, the high proportion in list A is explained by duplication of small proteins (e.g. 56% of proteins in this category are Esx and PE proteins).
This absence of synteny could be explained by duplication events and subsequent gene losses or by the translocation of the focal genes.
Moreover, the presence of multiple genes of the same species within single phylogenetic groups can be explained by duplication events occurred either after the separation of the angiosperms from the briophytes or later, after the diversification of monocots and dicots.
This discrepancy can potentially be explained by duplication of some loci in Cyprinus carpio L., and a model that shows how duplication can increase heterozygosity estimates for microsatellites but not for AFLP loci is discussed.
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The mechanisms of MITE amplification remain poorly understood; but for BuT2 MITES apparently, it could not be explained by duplications.
Multiple sequence alignment reveals that differences in the size of tenascin-W from various vertebrate classes can be explained by duplications of specific fibronectin type III domains.
D) Evidence of a dispersed duplication Although most of the PTP gene family expansion can be explained by duplications of entire segments, some examples of dispersed duplications involving a single gene could also be found.
The evolutionary significance of gene duplication is explained by the duplication-degeneration-complementation (DDC) model, which states that the probability of a duplicate gene to be preserved increases with the occurrence of degenerative mutations in its regulatory region [36].
We suggest that this can be explained by gene duplication.
This can for a large part be explained by inherent duplication features of indels.
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